Articles de revues : « Autoantibody reactivity »

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Biggs, Catherine M., Svetlana Kostjukovits, Kerry Dobbs, Saila Laakso, Paula Klemetti, Helena Valta, Mervi Taskinen, Outi Mäkitie et Luigi D. Notarangelo. « Diverse Autoantibody Reactivity in Cartilage-Hair Hypoplasia ». Journal of Clinical Immunology 37, n^o 6 (19 juin 2017) : 508–10. http://dx.doi.org/10.1007/s10875-017-0408-4.

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Yu, Xuechen, Melanie Uhde, Peter Green et Armin Alaedini. « Autoantibodies in the Extraintestinal Manifestations of Celiac Disease ». Nutrients 10, n^o 8 (20 août 2018) : 1123. http://dx.doi.org/10.3390/nu10081123.

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Increased antibody reactivity towards self-antigens is often indicative of a disruption of homeostatic immune pathways in the body. In celiac disease, an autoimmune enteropathy triggered by the ingestion of gluten from wheat and related cereals in genetically predisposed individuals, autoantibody reactivity to transglutaminase 2 is reflective of the pathogenic role of the enzyme in driving the associated inflammatory immune response. Autoantibody reactivity to transglutaminase 2 closely corresponds with the gluten intake and clinical presentation in affected patients, serving as a highly useful biomarker in the diagnosis of celiac disease. In addition to gastrointestinal symptoms, celiac disease is associated with a number of extraintestinal manifestations, including those affecting skin, bones, and the nervous system. Investigations of these manifestations in celiac disease have identified a number of associated immune abnormalities, including B cell reactivity towards various autoantigens, such as transglutaminase 3, transglutaminase 6, synapsin I, gangliosides, and collagen. Clinical relevance, pathogenic potential, mechanism of development, and diagnostic and prognostic value of the various identified autoantibody reactivities continue to be subjects of investigation and will be reviewed here.

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Takeuchi, K., S. J. Turley, E. M. Tan et K. M. Pollard. « Analysis of the autoantibody response to fibrillarin in human disease and murine models of autoimmunity. » Journal of Immunology 154, n^o 2 (15 janvier 1995) : 961–71. http://dx.doi.org/10.4049/jimmunol.154.2.961.

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Abstract Fibrillarin, a component of the U3 RNP particle, is a target for the spontaneously arising autoantibodies in human scleroderma and a monoclonal autoantibody (72B9) derived from the autoimmune mouse strain (NZB x NZW) F1. Autoantibodies against fibrillarin can also be induced in H-2s mice by treatment with mercuric chloride (HgCl2). The objective of this study was to compare the spontaneously occurring anti-fibrillarin autoantibody response with the autoantibody response induced by HgCl2 treatment. Immunofluorescence microscopy on human HEp2, mouse 3T3, and Xenopus XIK-2 cells, immunoblotting with use of nuclear extract from human MOLT-4, mouse 3T3, and Xenopus XIK-2 cells, and immunoprecipitation with use of in vitro translation products of RNA transcripts from yeast fibrillarin cDNA were used in this analysis. Both spontaneous and induced autoantibodies displayed common reactivity in that, irrespective of the antigenic source, they gave the same nucleolar immunofluorescence pattern and a restricted immunoblotting reactivity targeting predominantly the 34-kDa protein fibrillarin. Immunoprecipitation of N- and C-terminal truncated fibrillarin constructs also demonstrated a common pattern of reactivity. All Abs precipitated a fragment comprising amino acids 1-312 but not a smaller fragment containing amino acids 1-257. The majority of sera could not precipitate an N-terminal truncated molecule consisting of amino acids 157-327. These immunoprecipitation experiments support recognition of a common epitope requiring both N- and C-regions, which may be exemplified by the reactivity of murine monoclonal anti-fibrillarin autoantibody 72B9. Our results indicate that spontaneous human and toxin-induced murine autoantibodies to fibrillarin share common reactivity against this highly conserved nucleolar protein.

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Sibanda, Elopy N., Margo Chase-Topping, Lorraine T. Pfavayi, Mark E. J. Woolhouse et Francisca Mutapi. « Evidence of a distinct group of Black African patients with systemic lupus erythematosus ». BMJ Global Health 3, n^o 5 (septembre 2018) : e000697. http://dx.doi.org/10.1136/bmjgh-2017-000697.

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BackgroundThe autoimmune disease systemic lupus erythematosus (SLE) occurs more frequently in patients of African descent with high morbidity and mortality. Current SLE diagnostic criteria including antinuclear antibody (ANA) reactivity are derived largely from non-African populations. This study characterises ANA reactivity patterns and relates them to SLE clinical presentation in Black African patients.MethodsSera from Black participants (61 patients with SLE and 100 controls) aged 1–81 years were analysed for reactivity against the antigens: uridine 1-ribonuclear protein, Smith uridine-1-5 ribonuclear protein antigen, soluble substance-A, recombinant Ro-52, soluble substance-B, Scl-70, cytoplasmic histidyl-tRNA synthetase antigen, proliferating cell nuclear antigen (PCNA), nucleosomes, ribonuclear P-protein, antimitochondrial antibody M2 (AMA-M2), histones, double-stranded DNA (dsDNA), centromere protein B and polymyositis–sclerosis overlap antigen.FindingsA significantly higher proportion (97%) of the 61 patients with SLE had detectable autoantibody reactivity compared with 15% of the 100 controls (p<0.001). The highest frequencies of autoantibody reactivity in patients with SLE were against the dsDNA antigen (41%) and PCNA (54%). Anti-PCNA and anti-dsDNA reactivity were mutually exclusive (p<0.001) giving rise to two distinct groups of Black African patients with SLE. The first group (n=25) had reactivity profiles consistent with international standard SLE definitions, including anti-dsDNA reactivity, and was 13 times more likely to present with joint symptoms. The larger, second group (n=34), characterised by anti-PCNA and anti-AMA-M2 reactivity, was nine times more likely to present with only cutaneous symptoms.InterpretationOur study demonstrates a need to extend autoantibody panels to include anti-PCNA in the diagnostic process of Black African patients and further refine the predictive values of the reactivity to different antigens to differentiate SLE syndromes in African populations.

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Dellavance, Alessandra, Danielle C. Baldo, Bing Zheng, Rodrigo A. Mora, Marvin J. Fritzler, Falk Hiepe, Johan Rönnelid et al. « Establishment of an international autoantibody reference standard for human anti-DFS70 antibodies : proof-of-concept study for a novel Megapool strategy by pooling individual specific sera ». Clinical Chemistry and Laboratory Medicine (CCLM) 57, n^o 11 (25 octobre 2019) : 1754–63. http://dx.doi.org/10.1515/cclm-2019-0087.

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Abstract Background International autoantibody standards, traditionally based on material obtained from plasmapheresis of single subjects, represent individual immune response and may not comprehend the heterogeneity of the general population. The anti-DFS70 autoantibody yields a characteristic dense fine speckled (DFS) nuclear pattern on indirect immunofluorescence assay on HEp-2 cells (HEp-2 IFA) and speaks against autoimmunity. We propose a novel strategy for developing autoantibody reference standards, based on stepwise pooling of serum samples from hundreds of individuals with anti-DFS70 antibodies. Methods Within a 2-year period, serum samples were selected from routine HEp-2 IFA according to the following criteria: DFS HEp-2 IFA pattern at titer ≥1:640; anti-DFS70 reactivity in three analyte-specific tests (Western blot [WB], enzyme-linked immunosorbent assay [ELISA] and chemiluminescent immunoassay [CLIA]). Aliquots of individual samples were combined into progressively larger pools with stepwise validation of intermediary pools as for individual samples. Validated intermediary pools were merged into a final pool for lyophilization. Results A total of 741 validated samples yielded a 750 mL final pool that was lyophilized into thousands of 200 μL-aliquots. Reconstituted aliquots yielded the expected anti-DFS70 reactivity in ELISA, CLIA and WB, as well as high-titer DFS HEp-2 IFA pattern. The appropriate anti-DFS70 reactivity of the lyophilized pool was confirmed by seven international expert centers, using HEp-2 IFA, ELISA, WB and immunoprecipitation. Conclusions This proof-of-concept study provides an innovative and efficient strategy to build serum reference standards for autoantibody testing. The anti-DFS70 standard will integrate the panel of standards of Autoantibody Standardization Committee (ASC, www.autoab.org), contributing to education for proper assay validation and interpretation of the DFS pattern and other HEp-2 IFA patterns.

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Van Haren, Keith, Beren H. Tomooka, Brian A. Kidd, Brenda Banwell, Amit Bar-Or, Tanuja Chitnis, Silvia N. Tenembaum et al. « Serum autoantibodies to myelin peptides distinguish acute disseminated encephalomyelitis from relapsing– remitting multiple sclerosis ». Multiple Sclerosis Journal 19, n^o 13 (23 avril 2013) : 1726–33. http://dx.doi.org/10.1177/1352458513485653.

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Background and objective: Acute disseminated encephalomyelitis (ADEM) and relapsing–remitting multiple sclerosis (RRMS) share overlapping clinical, radiologic and laboratory features at onset. Because autoantibodies may contribute to the pathogenesis of both diseases, we sought to identify autoantibody biomarkers that are capable of distinguishing them. Methods: We used custom antigen arrays to profile anti-myelin-peptide autoantibodies in sera derived from individuals with pediatric ADEM ( n = 15), pediatric multiple sclerosis (Ped MS; n = 11) and adult MS ( n = 15). Using isotype-specific secondary antibodies, we profiled both IgG and IgM reactivities. We used Statistical Analysis of Microarrays software to confirm the differences in autoantibody reactivity profiles between ADEM and MS samples. We used Prediction Analysis of Microarrays software to generate and validate prediction algorithms, based on the autoantibody reactivity profiles. Results: ADEM was characterized by IgG autoantibodies targeting epitopes derived from myelin basic protein, proteolipid protein, myelin-associated oligodendrocyte basic glycoprotein, and alpha-B-crystallin. In contrast, MS was characterized by IgM autoantibodies targeting myelin basic protein, proteolipid protein, myelin-associated oligodendrocyte basic glycoprotein and oligodendrocyte-specific protein. We generated and validated prediction algorithms that distinguish ADEM serum (sensitivity 62–86%; specificity 56–79%) from MS serum (sensitivity 40–87%; specificity 62–86%) on the basis of combined IgG and IgM anti-myelin autoantibody reactivity to a small number of myelin peptides. Conclusions: Combined profiles of serum IgG and IgM autoantibodies identified myelin antigens that may be useful for distinguishing MS from ADEM. Further studies are required to establish clinical utility. Further biological assays are required to delineate the pathogenic potential of these antibodies.

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Pilyugin, Maxim, Magdalena Ratajska, Maciej Stukan, Nicole Concin, Robert Zeillinger et Irmgard Irminger-Finger. « BARD1 Autoantibody Blood Test for Early Detection of Ovarian Cancer ». Genes 12, n^o 7 (25 juin 2021) : 969. http://dx.doi.org/10.3390/genes12070969.

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Background: Ovarian cancer (OC) is the most lethal gynaecological cancer. It is often diagnosed at an advanced stage with poor chances for successful treatment. An accurate blood test for the early detection of OC could reduce the mortality of this disease. Methods: Autoantibody reactivity to 20 epitopes of BARD1 and concentration of cancer antigen 125 (CA125) were assessed in 480 serum samples of OC patients and healthy controls. Autoantibody reactivity and CA125 were also tested for 261 plasma samples of OC with or without mutations in BRCA1/2, BARD1, or other predisposing genes, and healthy controls. Lasso statistic regression was applied to measurements to develop an algorithm for discrimination between OC and controls. Findings and interpretation: Measurement of autoantibody binding to a number of BARD1 epitopes combined with CA125 could distinguish OC from healthy controls with high accuracy. This BARD1-CA125 test was more accurate than measurements of BARD1 autoantibody or CA125 alone for all OC stages and menopausal status. A BARD1-CA125-based test is expected to work equally well for average-risk women and high-risk women with hereditary breast and ovarian cancer syndrome (HBOC). Although these results are promising, further data on well-characterised clinical samples shall be used to confirm the potential of the BARD1-CA125 test for ovarian cancer screening.

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Putterman, Chaim, Irene Blanco, Nicole Jordan, Vered Daniel-Carmi, Liron Belanis-Meirovich, Rachel Sorek, Ornit Cohen-Gindi et al. « Autoantibody profiling for Systemic Lupus Erythematosus diagnosis using the Immunarray CHIP™ (P4018) ». Journal of Immunology 190, n^o 1_Supplement (1 mai 2013) : 42.10. http://dx.doi.org/10.4049/jimmunol.190.supp.42.10.

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Abstract SLE is a chronic, recurrent, potentially fatal multisystem inflammatory disorder mainly affecting women. SLE patients produce antibodies to many different self-antigens. Yet, currently used serological markers for SLE are lacking in specificity and/or sensitivity. The aim of this study was to develop an improved diagnostic test by measuring and multiplexing specific autoantibody reactivities in SLE patients. Autoantibody reactivity profiles in serum samples collected from 97 SLE patients within three years of the diagnosis were compared with those of 56 healthy controls. Autoantibody profiles were determined using the ImmunArray iCHIP™ - a proprietary protein microarray technology that allows the display of antigens representing a wide range of SLE-associated biochemical pathways on a single chip. Using this novel platform, SLE patients could be differentiated from healthy subjects by a relatively small subset of auto-antigens and Epstein Barr Virus (EBV) antigens. The autoantibody reactivity profile that allowed SLE diagnosis with high sensitivity and specificity displayed differential response to known SLE-specific antigens, such as single-stranded DNA and EBV, and to several novel ones. Conclusion: An antibody profile for SLE diagnosis using a single multiplexed chip was successfully developed. This profile may differentiate between SLE patients and healthy individuals. Validation of this profile in additional patient samples is ongoing.

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Gabusi, Loi, Gissi, Spinelli, Bernardi et Buzzi. « Effectiveness of Topical Application of Heterologous Platelet Rich Plasma (PRP) in Oral Mucous Membrane Pemphigoid. A Report of a Case ». Proceedings 35, n^o 1 (12 décembre 2019) : 57. http://dx.doi.org/10.3390/proceedings2019035057.

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Mucous membrane pemphigoid (MMP) is a rare, predominantly mucosal subepithelialblistering disorder triggered by autoantibody reactivity to several basement membrane antigensincluding BP180, BP230, laminin 332, and type VII collagen [...]

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Caudie, Christiane. « Monoclonal IgM Autoantibody Reactivity in M-IgM Peripheral Neuropathy ». Clinical Reviews in Allergy & ; Immunology 19, n^o 1 (2000) : 7–18. http://dx.doi.org/10.1385/criai:19:1:7.

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Lampasona, V., M. Bearzatto, S. Genovese, E. Bosi, M. Ferrari et E. Bonifacio. « Autoantibodies in insulin-dependent diabetes recognize distinct cytoplasmic domains of the protein tyrosine phosphatase-like IA-2 autoantigen. » Journal of Immunology 157, n^o 6 (15 septembre 1996) : 2707–11. http://dx.doi.org/10.4049/jimmunol.157.6.2707.

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Abstract Protein tyrosine phosphatase-like IA-2 is a major autoantigen in insulin-dependent diabetes. It has been identified as both a specificity of cytoplasmic islet cell Abs and one of the precursors of the 40- and 37-kDa tryptic fragment islet autoantigens. To characterize autoantibody binding to IA-2 and determine whether humoral autoimmunity extends to other tyrosine phosphatases, we analyzed serum reactivity in 100 patients with insulin-dependent diabetes against different in vitro translated portions of the IA-2 protein as well as the tyrosine phosphatase domains of HPTPbeta and HPTPdelta. All autoantibody reactivity was confined to the cytoplasmic portion of IA-2 (amino acids 601-979). At least four epitopes were found. These were contained within amino acids 605 to 620 and 605 to 682 of the juxtamembrane region and within amino acids 777 to 937 and 687 to 979 in the IA-2 tyrosine phosphatase-like domain. Footprinting studies confirmed the presence of multiple epitopes. Fifty-six percent of sera with IA-2 Abs bound epitopes within the juxtamembrane region, and 83% bound epitopes in the tyrosine phosphatase-like domain; 39% had Abs to both regions. No reactivity against the IA-2 ectodomain or the tyrosine phosphatase domains of HPTPbeta and HPTPdelta was found. These data suggest that the cytoplasmic region, in particular the tyrosine phosphatase-like domain, is the major target of IA-2 Abs in insulin-dependent diabetes, and that autoantibody reactivity is specific for IA-2 or IA-2-like molecules.

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ruff, william, Alexander S. Roth, Carina Anja Dehner, Silvio Manfredo Vieira, Andrew Goodman et Martin A. Kriegel. « Autoantibody cross-reactivity with a microbial protein from a prevalent human gut commensal in antiphospholipid syndrome ». Journal of Immunology 198, n^o 1_Supplement (1 mai 2017) : 58.4. http://dx.doi.org/10.4049/jimmunol.198.supp.58.4.

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Abstract Given the vast antigenic source of the gut microbiota, we hypothesized that human gut commensal bacteria induce and sustain autoreactivity via cross-reactivity. As a paradigm, we studied the antiphospholipid syndrome (APS), which is a serious autoimmune clotting disorder of unknown etiology but with a well-defined major autoantigen, b2-glycoprotein I (b2GPI). Infectious triggers are implicated in transient autoantibody production, but the persistent stimuli for anti-b2GPI antibodies remain unknown. To this end, we characterized b2GPI-specific monoclonal autoantibody reactivity to an in silico identified candidate commensal, Roseburia intestinalis (R.int), that is abundant in human stool from APS patients as detected by a species-specific PCR. Using an APS-derived monoclonal antibody, P1-117, that binds to the major B cell epitope in domain I of b2GPI (RGGMR), we tested for cross-reactivity to anaerobically cultured R.int and its candidate cross-reactive R.int protein (WP_006857340.1). P1-117 bound significantly to R.int lysates whereas a control antibody specific for another epitope within b2GPI did not. Further, P1-117 displayed significant binding to the recombinantly expressed R.int cross-reactive candidate protein. BALB/cJ mice immunized with whole heat-killed R.int displayed significant cross-reactive splenocytes and low titers of cross-reactive IgG autoantibodies. In conclusion, we present here in vitro and in vivo studies supporting cross-reactivity of pathogenic b2GPI-specific autoantibody with a common gut commensal. This study provides a concept for persistently colonizing gut commensals as chronic cross-reactive triggers in genetically susceptible autoimmune hosts such as APS patients.

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Martin, T., R. Crouzier, J. C. Weber, T. J. Kipps et J. L. Pasquali. « Structure-function studies on a polyreactive (natural) autoantibody. Polyreactivity is dependent on somatically generated sequences in the third complementarity-determining region of the antibody heavy chain. » Journal of Immunology 152, n^o 12 (15 juin 1994) : 5988–96. http://dx.doi.org/10.4049/jimmunol.152.12.5988.

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Abstract SMI is a previously characterized IgM kappa polyreactive (natural) autoantibody. The variable regions of the heavy and light chains of SMI are respectively encoded by a nonmutated VH1 gene, designated 51p1, and a conserved nonmutated V kappa gene, designated Humkv325. These V genes seem to be over-represented in the autoimmune and fetal B cell repertoires, and to be frequently expressed in malignant B cells during certain lymphoid proliferations such as chronic lymphocytic leukemia. Polyreactive natural autoantibodies are thought to rely mainly on the use of such V genes in germ-line configuration. However, this model underestimates the contribution of the somatically generated heavy chain third complementarity-determining region (HCDR3) to autoantibody specificity. We used oligonucleotide site-directed mutagenesis to permute the sequence of the SMI-HCDR3 to generate a family of mutant proteins, each of which differed from the original SMI-IgM kappa by one amino acid residue. This allowed us to examine the relative contribution of selected amino acid residues in this region to the binding affinity of SMI against a panel of self-Ags. We found that a single amino acid substitution within the HCDR3 could dramatically alter the specificity of this autoantibody. Some substitutions abrogated the reactivity with all the tested Ags, whereas others changed the affinity or spectrum of reactivity for certain self-Ags. These results demonstrate that the autoantibody-binding activity of these conserved autoantibody-associated germ-line V genes is dependent upon heavy chain junctional sequences that are generated somatically during Ig gene rearrangement.

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Frostegård, J., C. Hellström, P. Nilsson, A. G. Frostegård et S. Ajeganova. « Autoantibody profiling reveals four protein candidate autoantigens associated with systemic lupus erythematosus ». Lupus 27, n^o 10 (24 juillet 2018) : 1670–78. http://dx.doi.org/10.1177/0961203318788153.

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Objectives In systemic lupus erythematosus (SLE) there are typically many autoantibodies. The disease heterogeneity could be better understood with discovery of phenotype-specific antigens targeted by autoantibodies. We here aimed to identify novel autoantigens potentially related to SLE disease and a major complication, atherosclerosis. Methods Antigen microarrays were used to profile IgG autoantibody reactivity against 77 protein fragments (20–140 amino acids (aa) long, median 89 aa) produced within the Human Protein Atlas project, in serum samples from SLE patients ( n = 107) and age- and sex-matched population-based controls ( n = 107). Common carotid intima-media thickness, plaque occurrence and echogenicity were determined by B-mode ultrasound. Results We determined significant differences between patients and controls in IgG reactivity against four proteins. In patients compared to controls, there was an increase of IgG reactivity against zinc finger protein 688 (ZNF688), early B cell factor 2 (EBF2), crystallin, alpha B (CRYAB) and tumor necrosis factor receptor superfamily member 13C (TNFRSF13C). Of these four antigens, only anti-ZNF688 was associated with carotid atherosclerosis (plaque occurrence) and vulnerable plaques in SLE. There was a weak association between anti-EBF2 and SLE disease activity but no significant associations were determined for other measured IgG reactivity. Conclusions In this discovery screening we here demonstrate new candidate autoantigens with differential reactivity (reflecting autoantibody levels) in SLE patients and in controls and in relation to atherosclerosis in SLE.

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Ramirez-Celis, Alexandra, Martin Becker, Miriam Nuño, Joseph Schauer, Nima Aghaeepour et Judy Van de Water. « Risk assessment analysis for maternal autoantibody-related autism (MAR-ASD) : a subtype of autism ». Molecular Psychiatry 26, n^o 5 (22 janvier 2021) : 1551–60. http://dx.doi.org/10.1038/s41380-020-00998-8.

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AbstractThe incidence of autism spectrum disorder (ASD) has been rising, however ASD-risk biomarkers remain lacking. We previously identified the presence of maternal autoantibodies to fetal brain proteins specific to ASD, now termed maternal autoantibody-related (MAR) ASD. The current study aimed to create and validate a serological assay to identify ASD-specific maternal autoantibody patterns of reactivity against eight previously identified proteins (CRMP1, CRMP2, GDA, NSE, LDHA, LDHB, STIP1, and YBOX) that are highly expressed in developing brain, and determine the relationship of these reactivity patterns with ASD outcome severity. We used plasma from mothers of children diagnosed with ASD (n = 450) and from typically developing children (TD, n = 342) to develop an ELISA test for each of the protein antigens. We then determined patterns of reactivity a highly significant association with ASD, and discovered several patterns that were ASD-specific (18% in the training set and 10% in the validation set vs. 0% TD). The three main patterns associated with MAR ASD are CRMP1 + GDA (ASD% = 4.2 vs. TD% = 0, OR 31.04, p = <0.0001), CRMP1 + CRMP2 (ASD% = 3.6 vs. TD% = 0, OR 26.08, p = 0.0005) and NSE + STIP1 (ASD% = 3.1 vs. TD% = 0, OR 22.82, p = 0.0001). Additionally, we found that maternal autoantibody reactivity to CRMP1 significantly increases the odds of a child having a higher Autism Diagnostic Observation Schedule (ADOS) severity score (OR 2.3; 95% CI: 1.358–3.987, p = 0.0021). This is the first report that uses machine learning subgroup discovery to identify with 100% accuracy MAR ASD-specific patterns as potential biomarkers of risk for a subset of up to 18% of ASD cases in this study population.

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Frontzek, Karl, Manfredi Carta, Marco Losa, Mirka Epskamp, Georg Meisl, Alice Anane, Jean-Philippe Brandel et al. « Autoantibodies against the prion protein in individuals with PRNP mutations ». Neurology 95, n^o 14 (25 février 2020) : e2028-e2037. http://dx.doi.org/10.1212/wnl.0000000000009183.

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ObjectiveTo determine whether naturally occurring autoantibodies against the prion protein are present in individuals with genetic prion disease mutations and controls, and if so, whether they are protective against prion disease.MethodsIn this case–control study, we collected 124 blood samples from individuals with a variety of pathogenic PRNP mutations and 78 control individuals with a positive family history of genetic prion disease but lacking disease-associated PRNP mutations. Antibody reactivity was measured using an indirect ELISA for the detection of human immunoglobulin G1–4 antibodies against wild-type human prion protein. Multivariate linear regression models were constructed to analyze differences in autoantibody reactivity between (1) PRNP mutation carriers vs controls and (2) asymptomatic vs symptomatic PRNP mutation carriers. Robustness of results was examined in matched cohorts.ResultsWe found that antibody reactivity was present in a subset of both PRNP mutation carriers and controls. Autoantibody levels were not influenced by PRNP mutation status or clinical manifestation of prion disease. Post hoc analyses showed anti-PrPC autoantibody titers to be independent of personal history of autoimmune disease and other immunologic disorders, as well as PRNP codon 129 polymorphism.ConclusionsPathogenic PRNP variants do not notably stimulate antibody-mediated anti-PrPC immunity. Anti-PrPC immunoglobulin G autoantibodies are not associated with the onset of prion disease. The presence of anti-PrPC autoantibodies in the general population without any disease-specific association suggests that relatively high titers of naturally occurring antibodies are well-tolerated.Clinicaltrials.gov identifierNCT02837705.

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McHeyzer-Williams, M. G., et G. J. Nossal. « Clonal analysis of autoantibody-producing cell precursors in the preimmune B cell repertoire. » Journal of Immunology 141, n^o 12 (15 décembre 1988) : 4118–23. http://dx.doi.org/10.4049/jimmunol.141.12.4118.

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Abstract Evidence for anti-self-reactivity in the preimmune B cell repertoire has been well documented. The present study aimed to determine the frequency of antibody-forming cell precursors in this repertoire whose Ig V regions impart reactivity to "self" or autologous Ag. Clones were activated in vitro with LPS and their secreted IgM antibody was assayed for reactivity by direct binding to cell surface or intracellular Ag. An IL-4-containing lymphokine mixture was added to the clonal cultures to induce the secretion of IgG1. The reactivity of secreted IgG1 with Ag would more closely resemble the binding required to activate B cells through their monomeric surface IgM and/or IgD. The results indicate a high frequency of precursors secreting IgM with reactivity to intracellular Ag, namely 1 in 37 +/- 6 B cells, with a marked paucity of response to cell surface molecules. The repertoire was markedly deficient in precursors secreting IgG1 able to bind to intracellular Ag, with only one clone detected by the screening of 3.0 x 10(6) spleen cells. No positives were detected for cell surface Ag. This suggested that the frequency of clones in the preimmune repertoire that express IgR with sufficient affinity to bind "self" molecules must be very low.

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Weisbart, R. H., A. L. Wong, D. Noritake, A. Kacena, G. Chan, C. Ruland, E. Chin, I. S. Chen et J. D. Rosenblatt. « The rheumatoid factor reactivity of a human IgG monoclonal autoantibody is encoded by a variant V kappa II L chain gene. » Journal of Immunology 147, n^o 8 (15 octobre 1991) : 2795–801. http://dx.doi.org/10.4049/jimmunol.147.8.2795.

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Abstract To determine the genetic and molecular basis for rheumatoid factor (RF) autoantibody reactivity in patients with destructive, erosive arthritis, we established a human lymphoblastoid cell line (hRF-1) from a patient with polyarthritis that produced an IgG RF mAb, mAb hRF-1. Studies of isolated H and L chains showed that the specificity of RF reactivity is conferred by mAb hRF-1 L chains. The L chain gene was cloned from a cDNA library prepared from hRF-1 cells. The nucleotide sequence was similar to known V kappa II L chains except for a two nucleotide change corresponding to a change of two amino acids in an invariable region of FR3. A germ-line gene with one of the nucleotide changes was identified by polymerase chain reaction in multiple cell lines, including K562 that does not rearrange Ig genes, but the other nucleotide change appeared to be due to mutation. Either or both of these amino acid changes may contribute to the RF reactivity, because an antibody with the same V kappa II L chain except for these two amino acid changes in FR3 did not have RF reactivity. The RF reactivity of isolated L chains from mAb hRF-1 was confirmed by transfecting COS cells with an expression vector encoding the hRF-1 kappa-chain and showing that the secreted k-chains had RF reactivity. Expression of this variant V kappa II L chain gene may form the basis for RF autoantibody reactivity in some patients.

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Chiloiro, Sabrina, Ettore Domenico Capoluongo, Flavia Angelini, Feliciana Mariotti, Giuseppe Grande, Egidio Stigliano, Federica Vincenzoni et al. « Autoantibody reactivity profile of primary autoimmune hypophysitis patients : preliminary results ». Endocrine 76, n^o 1 (19 novembre 2021) : 224–27. http://dx.doi.org/10.1007/s12020-021-02937-1.

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Dang, Chuan V., Eng M. Tan et Jolinda A. Traugh. « Myositis autoantibody reactivity and catalytic function of threonyl‐tRNA synthetase ». FASEB Journal 2, n^o 8 (mai 1988) : 2376–79. http://dx.doi.org/10.1096/fasebj.2.8.2452112.

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Moinzadeh, Pia, Svetlana I. Nihtyanova, Kevin Howell, Voon H. Ong et Christopher P. Denton. « Impact of Hallmark Autoantibody Reactivity on Early Diagnosis in Scleroderma ». Clinical Reviews in Allergy & ; Immunology 43, n^o 3 (19 juin 2012) : 249–55. http://dx.doi.org/10.1007/s12016-012-8331-1.

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Celis, Nora Alexandra Ramirez, et Judy Van de Water. « Risk assessment test for MAR ASD : a subtype of Autism ». Journal of Immunology 204, n^o 1_Supplement (1 mai 2020) : 58.3. http://dx.doi.org/10.4049/jimmunol.204.supp.58.3.

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Abstract Background Autism spectrum disorder (ASD) is an important health issue and affects 1 in 59 children in the US. Prior studies found that maternal autoantibody related autism (MAR ASD) is thought to be responsible for ~20% of ASD cases. We aimed to create a robust assay to identify ASD-specific autoantibody patterns of reactivity against the previously identified brain antigens CRMP1, CRMP2, GDA, LDHA, LDHB, NSE, STIP1, and YBOX1 in the blood of mothers whose children have ASD and determine their relationship with ASD behavioral outcome. Methods We obtained plasma enrolled in the CHARGE study from mothers of children diagnosed with ASD (n=481) and control mothers of typically developing children (TD, n=377). Maternal plasma was probed against the eight antigens by ELISA and WB. We then determined patterns of reactivity that had a strong association with ASD by permutation analysis. Results We found several ASD specific patters of reactivity (positives for several antigens) in 16% of the ASD samples and 0% in the TD group. From those, 4 patterns of reactivity were statistically significant using Fisher’s exact test 0.05% showing a significant association of having autoantibodies against a combination of those antigens and a higher risk of having a child with MAR ASD. Also, preliminary studies indicate a positive correlation between having reactivity to multiple antigens and higher Autism Severity Scores (ADOS composite). Conclusion We developed the first risk assessment test to predict ASD with 100% specificity based on reactivity to different combinations of brain antigens. We are currently working on the development of multiple MAR ASD animal models.

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Masouredis, SP, MJ Branks et EJ Victoria. « Antiidiotypic IgG crossreactive with Rh alloantibodies in red cell autoimmunity ». Blood 70, n^o 3 (1 septembre 1987) : 710–15. http://dx.doi.org/10.1182/blood.v70.3.710.710.

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Abstract IgG autoantibodies eluted from RBCs of antiglobulin positive normal blood donors contained at least two antibody populations, an IgG autoantibody (Ab 1), and an IgG population (Ab 2) that agglutinated RBCs coated with some Rh(D) alloantibodies. Eight of 24 autoantibody eluates tested agglutinated 3 of 10 anti-Rh(D) sensitized RBCs. The agglutinating activity was inhibited specifically by preincubation of the autoantibody eluate with the reactive anti-D. The reaction did not require the Fc domain of the anti-Rh(D), since autoantibody eluates agglutinated RBCs coated with F(ab')2 prepared from the reactive anti-D sera. These findings indicate that the RBCs of some antiglobulin- positive blood donors contain an immunoglobulin auto-antiidiotype (Ab 2) against the RBC autoantibody (Ab 1) which is demonstrable through its cross-reactivity with selected Rh(D) alloantibodies. Identification of auto-antiidiotypes in RBC autoimmunity lends support to the idiotype- antiidiotype network hypothesis of immune regulation and is consistent with the bizarre and complex serology of autoimmune hemolytic anemia. The absence of clinical hemolysis in antiglobulin-positive normal blood donors suggests that immunoglobulin idiotype-antiidiotype interactions may play a role in modulating the effects of RBC autoimmunity.

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Masouredis, SP, MJ Branks et EJ Victoria. « Antiidiotypic IgG crossreactive with Rh alloantibodies in red cell autoimmunity ». Blood 70, n^o 3 (1 septembre 1987) : 710–15. http://dx.doi.org/10.1182/blood.v70.3.710.bloodjournal703710.

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IgG autoantibodies eluted from RBCs of antiglobulin positive normal blood donors contained at least two antibody populations, an IgG autoantibody (Ab 1), and an IgG population (Ab 2) that agglutinated RBCs coated with some Rh(D) alloantibodies. Eight of 24 autoantibody eluates tested agglutinated 3 of 10 anti-Rh(D) sensitized RBCs. The agglutinating activity was inhibited specifically by preincubation of the autoantibody eluate with the reactive anti-D. The reaction did not require the Fc domain of the anti-Rh(D), since autoantibody eluates agglutinated RBCs coated with F(ab')2 prepared from the reactive anti-D sera. These findings indicate that the RBCs of some antiglobulin- positive blood donors contain an immunoglobulin auto-antiidiotype (Ab 2) against the RBC autoantibody (Ab 1) which is demonstrable through its cross-reactivity with selected Rh(D) alloantibodies. Identification of auto-antiidiotypes in RBC autoimmunity lends support to the idiotype- antiidiotype network hypothesis of immune regulation and is consistent with the bizarre and complex serology of autoimmune hemolytic anemia. The absence of clinical hemolysis in antiglobulin-positive normal blood donors suggests that immunoglobulin idiotype-antiidiotype interactions may play a role in modulating the effects of RBC autoimmunity.

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Edberg, J. C., et R. P. Taylor. « Quantitative aspects of lupus anti-DNA autoantibody specificity. » Journal of Immunology 136, n^o 12 (15 juin 1986) : 4581–87. http://dx.doi.org/10.4049/jimmunol.136.12.4581.

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Abstract In this study we have attempted to define the cross-reactive potential of SLE anti-DNA antibodies (in 19 representative sera and plasmas) in both the solution phase and the solid phase. We used the Farr and RBC-CF solution phase assays to measure quantitatively the ability of a variety of negatively charged structurally unrelated molecules to inhibit antibody binding to both native DNA (nDNA) and denatured DNA (dDNA). The inhibitors used were of two types: 1) phospholipids (cardiolipin, phosphatidyl glycerol, and phosphatidic acid) and 2) repeating negatively charged molecules (poly-glutamic acid, heparin sulfate, and chondroitin sulfate). We found in both assays that the phospholipids could inhibit antibody binding to nDNA and dDNA, but a large excess (about 1500-fold) of these molecules was needed relative to DNA to achieve equivalent levels of inhibition. The repeating negatively charged molecules did not inhibit DNA binding at equivalent molar levels as the phospholipids; generally, at least a 10,000-fold excess was needed relative to the nucleic acids to achieve any appreciable inhibition. Results of a dDNA binding-inhibition solid-phase ELISA for cross-reactivity of the anti-DNA antibodies gave quite similar results. Finally, we found that eight of the SLE samples did have anti-cardiolipin antibodies, as demonstrated in a cardiolipin-based ELISA. These results suggest that previous reports describing an apparent cross-reactivity of anti-DNA antibodies may not represent physiologically relevant interactions between anti-DNA antibodies and non-nucleic acid antigens.

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Strugnell, R. A., W. F. Williams, G. Raines, J. S. Pedersen, L. P. Drummond, B. H. Toh et S. Faine. « Autoantibodies to creatine kinase in rabbits infected with Treponema pallidum. » Journal of Immunology 136, n^o 2 (15 janvier 1986) : 667–71. http://dx.doi.org/10.4049/jimmunol.136.2.667.

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Abstract Sera from rabbits infected intratesticularly with Treponema pallidum (Nichols) for 30 days were examined for autoantibody reactivity against muscle and testis extracts by Western immunoblotting. Syphilitic sera (30 day) reacted with an autoantigen of 43,000 daltons in muscle extracts. The antigen was shown to be creatine kinase (CK). Studies with the use of an anti-CK ELISA showed that the autoantibody to CK first appeared 3 wk after infection, declined by 7 wk infection, and was absent in rabbits "mock"-infected with heat-killed T. pallidum. CK activity was not detected in sonicated or intact, washed T. pallidum, suggesting that the antibody was not produced in response to treponemal CK.

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Rolim, Inês, Nádia Duarte, Gabriela Barata, João Costa, Luís Gardete-Correia, José Boavida, Rui Duarte et al. « Immunoglobulin M gene association with autoantibody reactivity and type 1 diabetes ». Immunogenetics 69, n^o 7 (22 mai 2017) : 429–37. http://dx.doi.org/10.1007/s00251-017-0999-1.

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Miller, D. J., et M. Rodriguez. « A monoclonal autoantibody that promotes central nervous system remyelination in a model of multiple sclerosis is a natural autoantibody encoded by germline immunoglobulin genes. » Journal of Immunology 154, n^o 5 (1 mars 1995) : 2460–69. http://dx.doi.org/10.4049/jimmunol.154.5.2460.

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Abstract Antibodies directed against self-Ags are frequently considered detrimental, and have been shown to play a pathogenic role in certain autoimmune diseases. However, the presence of autoreactive Abs in normal individuals suggests that some autoantibodies could participate in normal physiology. Our previous studies demonstrated that monoclonal autoantibodies SCH94.03 and SCH94.32, generated from the splenocytes of uninfected SJL/J mice injected with normal homogenized spinal cord, promote central nervous system remyelination when passively transferred into syngeneic mice chronically infected with Theiler's murine encephalomyelitis virus, an established experimental model of multiple sclerosis. In this study we show that these two monoclonal autoantibodies are identical, and have phenotypic characteristics of natural autoantibodies. By using a solid phase assay system, SCH94.03 and SCH94.32 showed reactivity toward several protein Ags and chemical haptens, with prominent reactivity toward spectrin, (4-hydroxy-3-nitrophenyl)acetyl, and fluorescein. Sequence analysis showed that both SCH94.03 and SCH94.32 were encoded by identical germline Ig light chain V kappa 10/J kappa 1 and heavy chain V23/DFL16.1/JH2 genes, with no definitive somatic mutations. These results indicate that a natural autoantibody participates in a beneficial physiologic response to central nervous system injury.

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Ludewig, Burkhard, Philippe Krebs, Helen Metters, Jutta Tatzel, Özlem Türeci et Ugur Sahin. « Molecular Characterization of Virus-induced Autoantibody Responses ». Journal of Experimental Medicine 200, n^o 5 (6 septembre 2004) : 637–46. http://dx.doi.org/10.1084/jem.20040358.

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Here we present a comprehensive molecular mapping of virus-induced autoimmune B cell responses obtained by serological identification of antigens by recombinant expression cloning analysis. Immunoscreening of cDNA expression libraries of various organs (lung, liver, and spleen) using sera from mice infected with cytopathic (vaccinia virus [VV]) or noncytopathic (lymphocytic choriomeningitis virus [LCMV]) viruses revealed a broad specificity of the elicited autoantibody response. Interestingly, the majority of the identified autoantigens have been previously described as autoantigens in humans. We found that induction of virus-induced autoantibodies of the immunoglobulin G class largely depends on the CD40–CD40L-mediated interaction between T and B cells. Furthermore, antibody titers against a number of autoantigens were comparable to the concomitantly induced antiviral antibody response. Comparison of serum reactivity against a selected panel of autoantigens after infection with VV, LCMV, or vesicular stomatitis virus showed that the different virus infections triggered distinct autoantibody responses, suggesting that virus infections may leave specific “autoantibody fingerprints” in the infected host.

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Chen, Yen-Fu, Ao-Ho Hsieh, Lian-Chin Wang, Kuang-Hui Yu et Chang-Fu Kuo. « Cytomegalovirus-Associated Autoantibody against TAF9 Protein in Patients with Systemic Lupus Erythematosus ». Journal of Clinical Medicine 10, n^o 16 (21 août 2021) : 3722. http://dx.doi.org/10.3390/jcm10163722.

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Background: Evidence indicates a causal link between cytomegalovirus (CMV) infection and the triggering of systemic lupus erythematosus (SLE). Animal studies have revealed that CMV phosphoprotein 65 (pp65) induces autoantibodies against nuclear materials and causes the autoantibody attack of glomeruli. IgG eluted from the glomeruli of CMVpp65-peptide-immunized mice exhibited cross-reactivity against dsDNA and TATA-box-binding protein associated factor 9 (TAF9). Whether the elevation of anti-TAF9 IgG is associated with anti-CMV reactivity in human lupus remains unclear. Methods: The sera from patients with rheumatic diseases, including ankylosing spondylitis (AS), gout, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sjögren syndrome (SS) were examined using ELISA for antibodies of CMV, CMVpp65, and TAF9. Results: In total, 83.8% of the rheumatic patients had acquired CMV infections. The SLE patients had a high prevalence of anti-CMV IgM. The highest seropositivity rates for anti-HCMVpp65 and anti-TAF9 IgG were observed in the SLE patients. Purified anti-CMVpp65 IgG from CMVpp65/TAF9 dual-positive SLE sera reacted to both TAF9 and dsDNA. An increased prevalence of proteinuria and low hemoglobin levels were found in CMV IgG- and CMVpp65 IgG-positive SLE patients. Conclusions: This observation suggests that immunity to CMVpp65 is associated with cross-reactivity with TAF9 and dsDNA and that it is involved in the development of clinical manifestations in SLE.

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Poulsen, T. B. G., D. Damgaard, M. M. Jørgensen, L. Senolt, J. Blackburn, C. H. Nielsen et A. Stensballe. « SAT0012 ANTIBODY REACTIVITY AGAINST NATIVE PROTEINS IN RHEUMATOID ARTHRITIS ». Annals of the Rheumatic Diseases 79, Suppl 1 (juin 2020) : 936.2–936. http://dx.doi.org/10.1136/annrheumdis-2020-eular.6124.

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Background:The majority of patients with rheumatoid arthritis (RA) produce autoantibodies against proteins that have undergone post-translational modfication, e.g. citrullination or carbamylation. There is growing evidence of their relevance and their potential utility to improve diagnosis, patient stratification, and prognosis for precision medicine. Investigating new autoantibody patterns may allow further stratification of patients and identifying subsets of patients that benefit from different treatment modalities. Following the discovery of high autoantibody reactivity against multiple modified proteins the interest in native targets decreased. Even though antibodies reacting with native proteins may also have a role in RA pathogenesis, their reactivity patterns are much less studied.Objectives:To identify novel native autoantigens in RA patients and elucidate patterns within autoantibody reactivity against native autoantigens.Methods:We investigated the reactivity of autoantibodies in plasma pools from 15 anti-CCP positive and 10 anti-CCP negative RA patients and 10 healthy donors against more than 1600 human proteins in native configuration using the Immunome high-density protein microarray.Results:We identified 86 native proteins that were recognized by IgG antibodies from anti-CCP positive RA patients and 76 native proteins recognized by IgG antibodies from anti-CCP negative RA patients, but not by antibodies from healthy donors. Examples of proteins recognized by both patient subgroups are calcium/calmodulin-dependent protein kinase type II subunits, histone deacetylases, keratin, and vimentin. Reactivity against the ribonucleic protein SSB was observed in anti-CCP negative RA patients only.Conclusion:Several human proteins in their native conformation are recognized by autoantibodies from anti-CCP positive as well as anti-CCP negative RA patients. In general, anti-CCP positive patients had higher autoantibody activity than anti-CCP negative patients and healthy donors.References:[1] Konig, M.F., Giles, J.T., Nigrovic, P.A., Andrade, F., 2016. Antibodies to native and citrullinated RA33 (hnRNP A2/B1) challenge citrullination as the inciting principle underlying loss of tolerance in rheumatoid arthritis. Ann. Rheum. Dis. 75, 2022–2028.[2] Zheng, Z., Mergaert, A.M., Fahmy, L.M., Bawadekar, M., Holmes, C.L., Ong, I.M., Bridges, A.J., Newton, M.A., Shelef, M.A., 2019. Disordered Antigens and Epitope Overlap Between Anti-Citrullinated Protein Antibodies and Rheumatoid Factor in Rheumatoid Arthritis. Arthritis Rheumatol. art.41074.[3] Sirotti, S., Generali, E., Ceribelli, A., Isailovic, N., De Santis, M., Selmi, C., 2017. Personalized medicine in rheumatology: the paradigm of serum autoantibodies. Autoimmun. Highlights 8.Acknowledgments :The Department of Clinical Immunology at Rigshospitalet Copenhagen is acknowledged for providing the healthy donor blood. The study is part of the PROCIT study financed by the Danish Council for Independent Research (grant no. DFF - 7016-00233). Moreover, the Obelske Family Foundation, the Svend Andersen Foundation, the Spar Nord Foundation and the Danish National Mass Spectrometry Platform for Functional Proteomics (PRO-MS; grant no. 5072-00007B) are acknowledged for grants to the analytical platform are acknowledged for the funding to enabling parts of this study.Disclosure of Interests:Thomas B.G. Poulsen: None declared, Dres Damgaard: None declared, Malene Møller Jørgensen: None declared, Ladislav Senolt: None declared, Jonathan Blackburn Shareholder of: Sengenics Corporation, Consultant of: Director of Sengenics Corporation, Employee of: Director of Sengenics Corporation, Claus Henrik Nielsen: None declared, Allan Stensballe: None declared

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Neu, N., K. W. Beisel, M. D. Traystman, N. R. Rose et S. W. Craig. « Autoantibodies specific for the cardiac myosin isoform are found in mice susceptible to Coxsackievirus B3-induced myocarditis. » Journal of Immunology 138, n^o 8 (15 avril 1987) : 2488–92. http://dx.doi.org/10.4049/jimmunol.138.8.2488.

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Abstract Several mouse strains are susceptible to immunopathic myocarditis after infection with Coxsackievirus B3 (CB3). This disease is associated with autoantibodies that are directed against myosin. In this study we characterized sera from CB3-infected mice for their reactivity with three different myosin isoforms (heart, skeletal muscle, and brain myosins) and for autoantibody isotype by using an ELISA. Competitive inhibition assays and absorption studies with various myosins demonstrated the presence of two autoantibody populations in sera of susceptible A.CA and A.SW mice. The first was specific for cardiac myosin and was mainly IgG. The second antibody population cross-reacted with heart, skeletal muscle, and brain myosin and was mainly IgM. B10.PL/SgSf and B10.A/SgSf mice, which do not develop immunopathic myocarditis, produced only the IgM autoantibody population cross-reactive with all three myosin isoforms. Because the heart-specific myosin autoantibodies were found exclusively in the mouse strains that developed immunopathic myocarditis, they can be considered a serologic marker for autoimmune heart disease.

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Vandormael, P., A. Pues, E. Sleurs, P. Verschueren et V. Somers. « FRI0596 NOVEL AUTOANTIBODY BIOMARKERS FOR THE PREDICTION OF THERAPY RESPONSE IN RHEUMATOID ARTHRITIS ». Annals of the Rheumatic Diseases 79, Suppl 1 (juin 2020) : 904.1–904. http://dx.doi.org/10.1136/annrheumdis-2020-eular.4184.

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Background:Rheumatoid arthritis (RA) is an autoimmune disorder that is characterized by chronic inflammation of the joint synovium and presence of autoantibodies in most patients. For RA, many treatments are currently available but each treatment will only induce disease remission in a subset of patients. Moreover, finding out which patients respond well to first-line therapy with classical synthetic disease modifying anti-rheumatic drugs (csDMARDs), still largely depends on trial and error.Objectives:In this study, we aim to find novel RA autoantibody biomarkers that predict therapy response to csDMARDs before the initiation of treatment.Methods:In the CareRA trial, a Flemish multicenter study of different treatment regimes, serum samples were collected from RA patients that did or did not show disease remission (DAS28(CRP)<2.6) in response to csDMARDs, combined with a step down glucocorticoid treatment. In our study, baseline samples, collected before the start of treatment, were used to determine predictive antibody reactivity. A cDNA phage display library, representing the antigens from RA synovial tissue, was constructed and screened for antibody reactivity in baseline serum samples of RA patients that failed to reach remission at week 16. Using enzyme-linked immunosorbent assays (ELISA), antibody reactivity against the identified antigens was initially determined in pooled baseline serum samples of RA patients that did (n=50) or did not (n=40) reach disease remission at week 16. Antigenic targets that showed increased antibody reactivity in pools from patients that did not reach disease remission, were further validated in individual serum samples of 69 RA patients that did not reach DAS28(CRP) remission at week 16, and 122 RA patients that did.Results:Screening and validation of antibody reactivity resulted in 41 novel antigens. The retrieved antigenic sequences correspond to (parts of) known proteins and to randomly formed peptides. A panel of 3 of these peptide antigens could be composed, whose baseline antibody reactivity correlated with lack of therapy response at week 16. Presence of antibodies against at least one of these 3 antigens was significantly higher in individual samples of RA patients that did not reach DAS28(CRP) remission (43 vs. 29%, p=0.041), or that failed to reach ACR 70 (42 vs. 26%, p=0.029) response criteria at week 16, compared to RA patients that did reach these respective criteria. In addition, RA patients which were positive for this antibody panel at baseline, also showed less DAS(CRP) remission at week 4 and week 8.Conclusion:We have identified a set of 3 antibody biomarkers that can predict failure of early disease remission after first-line RA therapy, which might contribute to personalized medicine decisions.Disclosure of Interests:Patrick Vandormael: None declared, Astrid Pues: None declared, Ellen Sleurs: None declared, Patrick Verschueren Grant/research support from: Pfizer unrestricted chair of early RA research, Speakers bureau: various companies, Veerle Somers Grant/research support from: Research grant from Pfizer and BMS

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Denomme, GA, JW Smith, JG Kelton et DA Bell. « A human monoclonal autoantibody to platelet glycoprotein IIb derived from normal human lymphocytes ». Blood 79, n^o 2 (15 janvier 1992) : 447–51. http://dx.doi.org/10.1182/blood.v79.2.447.447.

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Abstract Tonsillar lymphocytes from an otherwise healthy nonthrombocytopenic male child were fused with the lymphoblastoid cell line GM 4672. Twenty of 472 (4%) hybridomas had antiplatelet reactivity detected using intact platelets in an enzyme-linked immunosorbent assay. One hybridoma (STO 171) reacted to platelet glycoprotein IIb (integrin alpha IIb) as determined by radioimmunoprecipitation and immunoblotting. Antibody specificity was confirmed using immunodepletion experiments with isotypic antibodies derived from a mutlitransfused Glanzmann's thrombasthenic patient. The antibody reactivity was restricted to platelets and did not react with other integrin alpha-chain proteins expressed on granulocytes or cultured human brain-derived microvascular endothelial cells. These studies indicate that lymphocytes of normal, nonthrombocytopenic individuals have the genetic potential to produce antiplatelet autoantibodies.

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Denomme, GA, JW Smith, JG Kelton et DA Bell. « A human monoclonal autoantibody to platelet glycoprotein IIb derived from normal human lymphocytes ». Blood 79, n^o 2 (15 janvier 1992) : 447–51. http://dx.doi.org/10.1182/blood.v79.2.447.bloodjournal792447.

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Tonsillar lymphocytes from an otherwise healthy nonthrombocytopenic male child were fused with the lymphoblastoid cell line GM 4672. Twenty of 472 (4%) hybridomas had antiplatelet reactivity detected using intact platelets in an enzyme-linked immunosorbent assay. One hybridoma (STO 171) reacted to platelet glycoprotein IIb (integrin alpha IIb) as determined by radioimmunoprecipitation and immunoblotting. Antibody specificity was confirmed using immunodepletion experiments with isotypic antibodies derived from a mutlitransfused Glanzmann's thrombasthenic patient. The antibody reactivity was restricted to platelets and did not react with other integrin alpha-chain proteins expressed on granulocytes or cultured human brain-derived microvascular endothelial cells. These studies indicate that lymphocytes of normal, nonthrombocytopenic individuals have the genetic potential to produce antiplatelet autoantibodies.

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Meilof, J. F., A. Van der Lelij, L. A. Rokeach, S. O. Hoch et R. J. Smeenk. « Autoimmunity and filariasis. Autoantibodies against cytoplasmic cellular proteins in sera of patients with onchocerciasis. » Journal of Immunology 151, n^o 10 (15 novembre 1993) : 5800–5809. http://dx.doi.org/10.4049/jimmunol.151.10.5800.

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Abstract Onchocerciasis or "river blindness" is a vector-borne tropical disease resulting from infection with the filarial nematode Onchocerca volvulus. Disease manifestations include dermatitis, rheumatic complaints, and blindness. Recent findings have suggested an autoimmune etiology for the occurrence of chorioretinopathy, a disease of the eye which together with sclerosing keratoconjunctivitis is responsible for approximately 400,000 onchocerciasis-related cases of blindness. The identification of onchocerciasis as an important cause of tropical rheumatism prompted us to evaluate serologically the presence of systemic autoimmune disease in onchocerciasis patients and local controls from a hyperendemic area in Sierra Leone. In both groups there was a marked autoimmune response against cytoplasmic non-RNA-associated proteins consisting of autoantibodies against five major Ag with respective m.w. of 35, 51, 64, 83, and 110 kDa. These five proteins are novel autoantigens that could be distinguished from calreticulin, the human homologue of the onchocercal Ag RAL-1, and known autoantigens such as the 50-kDa La/SS-B or 52- and 60-kDa Ro/SS-A proteins by immunoblotting and ELISA assays. Furthermore, autoantibody reactivity against calreticulin was significantly higher in O. volvulus-infected individuals than in endemic controls. Autoantibody reactivity against the five major autoantigens, anti-calreticulin reactivity, and antibody reactivity against the 65-kDa arthritis-associated mycobacterial heat shock protein were intercorrelated as parts of an onchocerciasis-associated autoimmune response. The implication of autoimmunity in the disease pathogenesis of onchocerciasis could have important consequences for future research on therapeutical regimens, pathogenetic mechanisms, and serological diagnosis of onchocerciasis.

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Lourido, L., C. Ruiz-Romero, L. Collado, M. Hansson, L. Klareskog, R. Sjöberg, E. Pin, P. Nilsson et F. J. Blanco. « POS0392 PRESENCE OF FOUR SERUM AUTOANTIBODIES ASSOCIATES WITH THE ACPA STATUS IN EARLY RHEUMATOID ARTHRITIS ». Annals of the Rheumatic Diseases 80, Suppl 1 (19 mai 2021) : 425.3–426. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2514.

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Background:The presence of anti-citrullinated protein antibodies (ACPAs) is a hallmark of rheumatoid arthritis (RA) that precede the development of the disease by years and is used for its clinical diagnosis. However, there are RA subjects that test negative for ACPA and thus the early diagnosis on these patients may be delayed. Furthermore, the presence or absence of ACPA in RA supports the hypothesis that on these two subsets of patients underlie different pathogenesis and clinical outcomes.Objectives:In this work, we searched for serum autoantibodies useful to assist the early diagnosis of ACPA-seronegative RA and its management.Methods:We profiled the serum autoantibody repertoire of 80 ACPA-seronegative and 80 ACPA-seropositive RA subjects from the Swedish population-based Epidemiological Investigation of RA (EIRA) cohort. A suspension bead array platform built on protein fragments within Human Protein Atlas and selected from an initial untargeted screening using arrays containing 2660 total antigens was employed to identify IgG and IgA serum autoantibodies. A validation phase on antigen suspension bead arrays was carried out on another set of samples from EIRA containing 386 ACPA-seropositive, 358 ACPA-seronegative and 372 randomly selected control subjects of the same age and sex. A sample-specific threshold based on 20 times the median absolute deviation plus the median of all signals was selected to determine the reactivity of samples. The Wilcoxon rank sum test and Fisher’s test were applied for the comparison of autoantibody levels and reactivity frequencies between the groups.Results:Our data revealed four antigens associated with the ACPA status (Table 1). Testis-specific Y-encoded-like protein 4 (TSPYL4) showed significantly higher IgG reactivity frequency in ACPA-seronegative subjects compared to ACPA-seropositive (8% vs. 3%; P<0.05). Significant differences at IgG autoantibody levels (P<0.05) were also observed between ACPA-seronegative subjects and controls for this specific antigen. Significantly higher IgG autoantibody levels (P<0.05) towards another antigen, dual specificity mitogen-activated protein kinase kinase 6 (MAP2K6), were also observed in ACPA-seronegative subjects compared to ACPA-seropositive and controls. In contrast, we found significantly higher IgG autoantibody levels (P<0.05) in ACPA-seropositive individuals compared to ACPA-seronegative and controls towards two antigens, anosmin-1 (ANOS-1) and muscle related coiled-coil protein (MURC). ANOS-1 shows also significantly higher IgG reactivity frequency in ACPA-seropositive individuals compared to ACPA-seronegative and controls (22%, 9% and 6% respectively; P<0.05). Interestingly, three out of the four antigens discovered to be associated with the ACPA status in early RA are highly expressed in lungs and heart, two of the main extraarticular sites affected in RA. No significant differences were observed at IgA levels for any of the antigens analyzed.Table 1.Scheme of the different phases of the study, the features within each phase and the results. The reactivity to four antigens allows to distinguish ACPA-seronegative (ACPA-), ACPA seropositive (ACPA+) and controls.PhasesUntargeteddiscoveryTargeteddiscoveryTargetedvalidationNumber of samples80 ACPA-80 ACPA-358 ACPA-372 Controls80 ACPA+80 ACPA+386 ACPA+Antigen arrayplatformPlanararraysSuspensionbead array 1Suspensionbead array 2Number of antigens26606227Number of candidatebiomarkers6227 4 (TSPYL4,MAP2K6,ANOS1,MURC)Conclusion:Upon further validation in other early RA sample cohorts, our data suggest the measurement of these four autoantibodies may be useful for the early diagnosis of ACPA-seronegative RA and give insight into the pathogenesis of the different RA subsets.Characters from table content including title and footnotes:Disclosure of Interests:None declared

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Celis, Nora Alexandra Ramirez, et Judy Van de Water. « Evaluation of differential autoantibody profiles in gut and brain tissues in children with Autism Spectrum Disorder (ASD). » Journal of Immunology 206, n^o 1_Supplement (1 mai 2021) : 21.13. http://dx.doi.org/10.4049/jimmunol.206.supp.21.13.

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Abstract Autoimmunity is a comorbidity often associated with autism spectrum disorder (ASD), and a better understanding of immune dysbiosis and autism is crucial to identify differential ASD phenotypes and develop better biomarkers. We aimed to study autoantibody (aAb) reactivity to gut and brain tissues to find aAb profiles in children with autism that could serve to identify ASD subpopulations with biomarker potential. Methods: We used plasma from typically developing children (TD; n=149) and children diagnosed with ASD (n=208). To assess aAb reactivity, we probed plasma brain and gut tissues by Western blot. Results: While we found reactivity against brain (28% ASD and 32% TD), and gut (15% ASD and 11% TD) in both groups, we observed reactivity to antigens in defined molecular weight ranges in the gut tissue recognized by aAbs from the ASD subjects and not the TD samples. Further, some individuals had aAb reactivity to both brain and gut (8.6% ASD and 8% TD). These data are consistent with our previous studies against cerebellum tissue, where we reported aAb reactivity in both groups (ASD and TD), but some autoantibodies were differentially reactive in the ASD population. Conclusion: We identified aAbs reactive to brain and gut antigens in both TD and ASD children, with differential recognition of plasma from children with ASD to proteins in the gut extract. We are currently working on identification of the differentially recognized proteins in the gut tissue. Further, we can link our findings to the clinical data of these children, including reported GI issues. Such aAbs have the potential to serve as predictors of a subgroup of ASD individuals or facilitate a better understanding of the different sub-phenotypes of ASD based on differential aAb profiles.

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Gallin, M. Y., A. B. Jacobi, D. W. Büttner, O. Schönberger, T. Marti et K. D. Erttmann. « Human autoantibody to defensin : disease association with hyperreactive onchocerciasis (sowda). » Journal of Experimental Medicine 182, n^o 1 (1 juillet 1995) : 41–47. http://dx.doi.org/10.1084/jem.182.1.41.

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Chronic hyperreactive onchodermatitis (sowda) is a severe form of onchocerciasis observed in a subset of individuals infected with the filarial nematode Onchocerca volvulus. SDS-PAGE and immunoblot analyses of O. volvulus adult worm extracts were used to characterize the antigens of the marked antibody response of sowda patients. One 2.5-kD antigen was recognized by sera from all 35(100%) sowda patients that were studied. In comparison, only 7 of 44 (16%) patients with generalized onchocerciasis and 11 of 21 (52%) of exposed individuals with no microfilariae in skin snips and no signs of disease showed reactivity to this antigen. Microfilaricidal treatment of sowda patients with improvement of the clinical status was associated with a decrease or disappearance of antibodies to the 2.5-kD antigen. Amino acid sequencing of the antigen indicated identity to human defensins 1-3 of neutrophils. Defensin was demonstrated by immunohistochemical staining in onchocercal nodules on the surface of adult filariae and in the surrounding tissue. A similar staining pattern was observed for other proteins present in neutrophils such as myeloperoxidase, elastase, and the L-1 protein complex (MRP 8/MRP 14), indicating that neutrophils, macrophages, and their proteins predominate in the environment adjacent to the worms. These results demonstrate an association between the presence of autoantibodies to defensins and an infectious disease of known etiology. The association with a particular form of onchocerciasis, sowda, suggests a link between formation of autoantibodies to defensin and enhanced immune reactivity towards the parasite.

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Watts, R. A., W. Williams, S. Le Page, A. Norden, A. Soltys, G. Swana, I. Addison, F. C. Hay et D. A. Isenberg. « Analysis of autoantibody reactivity and common idiotype PR4 expression of myeloma proteins ». Journal of Autoimmunity 2, n^o 5 (octobre 1989) : 689–700. http://dx.doi.org/10.1016/s0896-8411(89)80007-1.

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Atkinson, M. A., D. L. Kaufman, D. Newman, A. J. Tobin et N. K. Maclaren. « Islet cell cytoplasmic autoantibody reactivity to glutamate decarboxylase in insulin-dependent diabetes. » Journal of Clinical Investigation 91, n^o 1 (1 janvier 1993) : 350–56. http://dx.doi.org/10.1172/jci116192.

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Souroujon, M., M. E. White-Scharf, J. Andreschwartz, M. L. Gefter et R. S. Schwartz. « Preferential autoantibody reactivity of the preimmune B cell repertoire in normal mice. » Journal of Immunology 140, n^o 12 (15 juin 1988) : 4173–79. http://dx.doi.org/10.4049/jimmunol.140.12.4173.

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Abstract Naturally occurring autoantibodies are frequently found in the sera of healthy individuals. They usually exhibit low binding affinities for autoantigens and often react with multiple antigenic determinants. To determine whether their frequencies have been overestimated by sensitive testing procedures, the germ-line B cell repertoire of strain A mice was examined for reactivity with a panel of auto- and foreign Ag. If the high frequencies of autoantibodies result from testing procedures, equally high frequencies would be expected for foreign Ag specificities detected in the same manner. The presence of specific autoantibodies was confirmed in this study by the disparate frequencies observed for antibodies reactive with individual Ag. The frequencies were highest for autoantigens associated with SLE, indicating a bias toward autoreactivity in the preimmune repertoire. Analysis of VH gene usage did not indicate any selection in V gene expression with autoreactivity.

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Naserke, Heike E., Anette-G. Ziegler, Vito Lampasona et Ezio Bonifacio. « Early Development and Spreading of Autoantibodies to Epitopes of IA-2 and Their Association with Progression to Type 1 Diabetes ». Journal of Immunology 161, n^o 12 (15 décembre 1998) : 6963–69. http://dx.doi.org/10.4049/jimmunol.161.12.6963.

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Abstract Autoimmunity precedes clinical type 1 diabetes, and indicators of maturing autoimmune responses may be useful markers for disease prediction. To study this, epitope maturation of autoantibodies to the related protein tyrosine phosphatase (PTP)-like autoantigens IA-2 and IA-2β was examined in sequential samples from birth in a cohort of 21 offspring developing multiple islet autoantibodies and a similar cohort of 48 relatives of patients with type 1 diabetes recruited at an older age. Initial reactivity in offspring was heterogeneous against the IA-2 juxtamembrane region (10/21) and PTP domains (13/21), and both specificity and extent of initial IA-2/IA-2β autoantibodies were associated with HLA class II genotype. Intra-IA-2 epitope spreading and/or intermolecular spreading to IA-2β epitopes were observed in seven offspring. In contrast, in older relatives, IA-2/IA-2β Ab reactivity was stable and spreading rare. Development of diabetes in children was associated with the presence of Abs to the IA-2 juxtamembrane region (risk by age 5 yr, 52% vs 0% in those with PTP domain Abs only; p < 0.02), and 5 of 26 relatives who developed diabetes had IA-2 Abs only against the juxtamembrane region. The findings show that autoantibody reactivity to IA-2/IA-2β is dynamic in the young, show that the juxtamembrane region of IA-2 is an early IA-2 autoantibody target, and suggest that these Abs are a risk factor for development of type 1 diabetes in infancy.

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Teitsma, Xavier M., Jenny Devenport, Johannes W. G. Jacobs, Attila Pethö-Schramm, Michelle E. A. Borm, Petra Budde, Johannes W. J. Bijlsma et Floris P. J. G. Lafeber. « Comprehensive exploratory autoantibody profiling in patients with early rheumatoid arthritis treated with methotrexate or tocilizumab ». PLOS ONE 15, n^o 12 (10 décembre 2020) : e0241189. http://dx.doi.org/10.1371/journal.pone.0241189.

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Background We sought to identify immunoglobin G autoantibodies predictive of early treatment response to methotrexate, the recommended first-line therapy for patients with newly diagnosed rheumatoid arthritis, and to the interleukin-6 receptor inhibitor biologic tocilizumab, initiated as the first disease-modifying anti-rheumatic drug. Materials and methods In baseline sera of a subset of patients with newly diagnosed rheumatoid arthritis in the U-Act-Early study, selected based on specific responder/non-responder criteria using the Disease Activity Score assessing 28 joints (DAS28) within the first 20 weeks, we measured immunoglobin G antibody reactivity against 463 protein antigens and performed supervised cluster analysis to identify predictive autoantibodies for treatment response. The analysis subset comprised 56 patients in the methotrexate arm (22 responders, 34 non-responders) and 50 patients in the tocilizumab arm (34 responders, 16 non-responders). For comparison, these analyses were also performed in 50 age- and gender-matched healthy controls. Results Increased reactivity in responders versus non-responders was found in the methotrexate arm against two antigens—DOT1-like histone lysine methyltransferase (p = 0.009) and tropomyosin (p = 0.003)—and in the tocilizumab arm against one antigen—neuro-oncological ventral antigen 2 (p = 0.039). Decreased reactivity was detected against two antigens in the methotrexate arm—G1 to S phase transition 2 (p = 0.023) and the zinc finger protein ZPR1 (p = 0.021). Reactivity against the identified antigens was not statistically significant in either treatment arm for patients with rheumatoid factor–positive versus–negative or anti-cyclic citrullinated test–positive versus test–negative rheumatoid arthritis (p ≥ 0.06). Conclusions Comprehensive profiling of baseline sera revealed several novel immunoglobin G autoantibodies associated with early treatment response to methotrexate and to tocilizumab in disease-modifying anti-rheumatic drug-naive patients with rheumatoid arthritis. These findings could eventually yield clinically relevant predictive markers, if corroborated in different patient cohorts, and may facilitate future benefit in personalised healthcare.

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Mintz, Paul J., Anna Cecilia Rietz, Marina Cardó-Vila, Michael G. Ozawa, Eleonora Dondossola, Kim-Anh Do, Jeri Kim et al. « Discovery and horizontal follow-up of an autoantibody signature in human prostate cancer ». Proceedings of the National Academy of Sciences 112, n^o 8 (9 février 2015) : 2515–20. http://dx.doi.org/10.1073/pnas.1500097112.

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In response to an urgent need for improved diagnostic and predictive serum biomarkers for management of metastatic prostate cancer, we used phage display fingerprinting to analyze sequentially acquired serum samples from a patient with advancing prostate cancer. We identified a peptide ligand, CTFAGSSC, demonstrating an increased recovery frequency over time. Serum antibody reactivity to this peptide epitope increased in the index patient, in parallel with development of deteriorating symptoms. The antigen mimicking the peptide epitope was identified as alpha-2–Heremans–Schmid glycoprotein, also known as fetuin-A. Metastatic prostate cancer cell lines and bone metastasis samples displayed robust fetuin-A expression, and we demonstrated serum immune reactivity to fetuin-A with concomitant development of metastatic castrate-resistant disease in a large cohort of prostate cancer patients. Whereas fetuin-A is an established tumor antigen in several types of cancer, including breast cancer, glioblastoma, and pancreas cancer, this report is to our knowledge the first study implicating fetuin-A in prostate cancer and indicating that autoantibodies specific for fetuin-A show utility as a prognostic indicator for prostate cancer patients prone to progress to metastatic disease.

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Laske, Christoph, Meta Zank, Reinhild Klein, Elke Stransky, Anil Batra, Gerhard Buchkremer et Klaus Schott. « Autoantibody reactivity in serum of patients with major depression, schizophrenia and healthy controls ». Psychiatry Research 158, n^o 1 (février 2008) : 83–86. http://dx.doi.org/10.1016/j.psychres.2006.04.023.

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Milchram, Lisa, Anita Fischer, Jasmin Huber, Regina Soldo, Daniela Sieghart, Klemens Vierlinger, Stephan Blüml, Günter Steiner et Andreas Weinhäusel. « Functional Analysis of Autoantibody Signatures in Rheumatoid Arthritis ». Molecules 27, n^o 4 (21 février 2022) : 1452. http://dx.doi.org/10.3390/molecules27041452.

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For the identification of antigenic protein biomarkers for rheumatoid arthritis (RA), we conducted IgG profiling on high density protein microarrays. Plasma IgG of 96 human samples (healthy controls, osteoarthritis, seropositive and seronegative RA, n = 24 each) and time-series plasma of a pristane-induced arthritis (PIA) rat model (n = 24 total) were probed on AIT’s 16k protein microarray. To investigate the analogy of underlying disease pathways, differential reactivity analysis was conducted. A total of n = 602 differentially reactive antigens (DIRAGs) at a significance cutoff of p < 0.05 were identified between seropositive and seronegative RA for the human samples. Correlation with the clinical disease activity index revealed an inverse correlation of antibodies against self-proteins found in pathways relevant for antigen presentation and immune regulation. The PIA model showed n = 1291 significant DIRAGs within acute disease. Significant DIRAGs for (I) seropositive, (II) seronegative and (III) PIA were subjected to the Reactome pathway browser which also revealed pathways relevant for antigen presentation and immune regulation; of these, seven overlapping pathways had high significance. We therefore conclude that the PIA model reflects the biological similarities of the disease pathogenesis. Our data show that protein array analysis can elucidate biological differences and pathways relevant in disease as well be a useful additional layer of omics information.

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Koh, Yi, David Nemazee, Robert Rickert, Marko Radic, Marilia Cascalho, Rafael Casellas, Argyrios Theofilopoulos et Dwight Kono. « FLEx-autoAb transgenic mice, a novel mouse model for studying peripheral tolerance to B cells that acquire self-reactivity following somatic hypermutation. (P4034) ». Journal of Immunology 190, n^o 1_Supplement (1 mai 2013) : 44.2. http://dx.doi.org/10.4049/jimmunol.190.supp.44.2.

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Abstract Uptake of nucleic acid-containing antigens by antigen receptors (BCRs) on B cells leading to endosomal TLR activation is thought to be critical for antinuclear autoantibody (ANA) production in lupus. However, it has been difficult to study this in peripheral B cells that acquire ANA specificity because current ANA BCR models are subjected to central tolerance mechanisms. To overcome this, we generated a FLEx-autoantibody (autoAb) transgenic model in which VH specificity can be changed from a non-self-reactive anti-nitrophenyl (NP) to anti-chromatin (3H9-56R) reactivity following Cre recombinase expression induced by tamoxifen (all B cells) or the activation induced cytidine deaminase promoter (during class-switch recombination/somatic hypermutation). In nonautoimmune C57BL/6 mice, B cells that acquire self-reactivity to chromatin were completely deleted after several days at all stages of development, although numbers of plasma cells were too low to analyze. Faslpr mutation enabled the development of only low levels of anti-id positive (56R+) plasma cells but did not rescue B cells at any other stages of development after tamoxifen. The provision of excess T cell help, through induction of chronic graft-versus-host disease in B6-Faslpr mice resulted in a marked increase in 56R+ plasma cells. These findings suggest that ANA-specificity and engagement of endogenous TLR is not sufficient to rescue autoreactive B cells even in mice with Fas deficiency.

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Mayer, Christian T., Jan P. Nieke, Anna Gazumyan, Melissa Cipolla, Qiao Wang, Thiago Y. Oliveira, Victor Ramos et al. « An apoptosis-dependent checkpoint for autoimmunity in memory B and plasma cells ». Proceedings of the National Academy of Sciences 117, n^o 40 (22 septembre 2020) : 24957–63. http://dx.doi.org/10.1073/pnas.2015372117.

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B lymphocytes acquire self-reactivity as an unavoidable byproduct of antibody gene diversification in the bone marrow and in germinal centers (GCs). Autoreactive B cells emerging from the bone marrow are silenced in a series of well-defined checkpoints, but less is known about how self-reactivity that develops by somatic mutation in GCs is controlled. Here, we report the existence of an apoptosis-dependent tolerance checkpoint in post-GC B cells. Whereas defective GC B cell apoptosis has no measurable effect on autoantibody development, disruption of post-GC apoptosis results in accumulation of autoreactive memory B cells and plasma cells, antinuclear antibody production, and autoimmunity. The data presented shed light on mechanisms that regulate immune tolerance and the development of autoantibodies.

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Meilof, J. F., I. M. E. Frohn-Mulder, P. A. Stewart, A. Szatmari, J. Hess, C. H. A. Veldhoven, R. J. T. Smeenk et A. J. G. Swaak. « Maternal Autoantibodies and Congenital Heart Block : No Evidence for the Existence of a Unique Heart Block-associated Anti-Ro/SS-A Autoantibody Profile ». Lupus 2, n^o 1_suppl (février 1993) : 239–46. http://dx.doi.org/10.1177/0961203393002001101.

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One of the rare examples of the transfer of autoimmune disease from mother to (unborn) child is the neonatal lupus syndrome. This syndrome comprises the development of fetal heart disease (congenital heart block) or neonatal skin rash and is specifically associated with maternal anti-Ro/SS-A autoantibodies. Previous studies have suggested that especially maternal autoantibody reactivity against the 52 kDa protein of the Ro/SS-A antigen and/or against the La/SS-B antigen is responsible for the development of congenital heart block (CHB). To determine the CHB-associated antibody response in more detail, we analysed the presence of autoantibodies in sera from mothers of children with isolated heart block. All 14 mothers of children with congenital heart block were positive for anti-Ro/SS-A antibodies. Remarkably, their antibody profile, including recognition of different Ro/SS-A proteins and autoantibody levels against these proteins, did not differ from anti-Ro/SS-A positive mothers of healthy children. In contrast, all 8 anti-Ro/SS-A negative mothers had children with acquired heart block. We conclude from our data that maternal anti-Ro/SS-A antibodies are essential for CHB but that fine analysis of this autoantibody response does not predict the occurrence of CHB.

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