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Journal articles on the topic 'HIGM1'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Takada, Yoko K., Michiko Shimoda та Yoshikazu Takada. "CD40L Activates Platelet Integrin αIIbβ3 by Binding to the Allosteric Site (Site 2) in a KGD-Independent Manner and HIGM1 Mutations Are Clustered in the Integrin-Binding Sites of CD40L". Cells 12, № 15 (2023): 1977. http://dx.doi.org/10.3390/cells12151977.

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CD40L is expressed in activated T cells, and it plays a major role in immune response and is a major therapeutic target for inflammation. High IgM syndrome type 1 (HIGM1) is a congenital functional defect in CD40L/CD40 signaling due to defective CD40L. CD40L is also stored in platelet granules and transported to the surface upon platelet activation. Platelet integrin αIIbβ3 is known to bind to fibrinogen and activation of αIIbβ3 is a key event that triggers platelet aggregation. Also, the KGD motif is critical for αIIbβ3 binding and the interaction stabilizes thrombus. Previous studies showed

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Vavassori, Valentina, Elisabetta Mercuri, Genni Marcovecchio, et al. "Towards Clinical Translation of Hematopoietic Cell Gene Editing for Treating Hyper-IgM Type 1." Blood 138, Supplement 1 (2021): 3978. http://dx.doi.org/10.1182/blood-2021-148572.

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Abstract Hyper-IgM Type 1 (HIGM1) is caused by mutations of CD40L, whose absence in CD4 T cells impairs signaling for B cell activation and Ig class-switching. Since unregulated CD40L expression leads to lymphoproliferations/lymphomas in the mouse model of the disease, gene correction must preserve the physiological regulation of the gene. Gene editing of either autologous T cells or hematopoietic stem cells (HSC) held promise for treating HIGM1. We developed a "one size fits all" editing strategy to insert a 5'-truncated corrective CD40L cDNA in the first intron of the native human gene, effe

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Callard, R. E., S. H. Smith, J. Herbert, et al. "CD40 ligand (CD40L) expression and B cell function in agammaglobulinemia with normal or elevated levels of IgM (HIM). Comparison of X-linked, autosomal recessive, and non-X-linked forms of the disease, and obligate carriers." Journal of Immunology 153, no. 7 (1994): 3295–306. http://dx.doi.org/10.4049/jimmunol.153.7.3295.

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Abstract Hyper-IgM syndrome is a rare immunodeficiency characterized by low or absent IgG, IgA, and IgE with normal or elevated levels of IgM. It can occur as an acquired or familial disorder with either X-linked or autosomal modes of inheritance. The X-linked form (HIGM1) is a result of mutations in the CD40 ligand (CD40L) gene, but the defect in non-X-linked forms of the disease (HIM) has not been determined. We show here that CD40L expression on activated T cells from non-X-linked patients can be detected by CD40Fc, 5c8 Mab, and anti-TRAP, whereas activated T cells from HIGM1 patients eithe

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Shimoda, Michiko, Yoko Takada, Emanual Maverakis, Brunhilde Felding, and Yoshikazu Takada. "CD40L acts as an allosteric activator of integrins for signal transduction independent of inside-out signaling." Journal of Immunology 206, no. 1_Supplement (2021): 24.04. http://dx.doi.org/10.4049/jimmunol.206.supp.24.04.

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Abstract CD40L plays a major role in immune response and is a target for inflammatory disease therapy. Besides CD40, CD40L binds to several integrins but their role in signaling is unclear. We showed that integrins αvβ3 and α5β1 bind to the CD40L trimeric interface through classical ligand binding site of integrins (site 1). Several CD40L mutants from HIGM1 (hyper-IgM syndrome type 1) patients were clustered in trimeric interface and defective in integrin binding, and in NF-κB and B cell activation, but still bound CD40 and acted as antagonists of CD40L signaling. Thus, integrins play a critic

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Life, P., J. F. Gauchat, V. Schnuriger, et al. "T cell clones from an X-linked hyper-immunoglobulin (IgM) patient induce IgE synthesis in vitro despite expression of nonfunctional CD40 ligand." Journal of Experimental Medicine 180, no. 5 (1994): 1775–84. http://dx.doi.org/10.1084/jem.180.5.1775.

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The induction of immunoglobulin E (IgE) switching in B cells requires at least two signals. The first is given by either of the soluble lymphokines interleukin 4 (IL-4) or IL-13, whereas the second is contact dependent. It has been widely reported that a second signal can be provided by the CD40 ligand (CD40L) expressed on the surface of T cells, mast cells, and basophils. A defect in the CD40L has been shown recently to be responsible for the lack of IgE, IgA, and IgG, characteristic of the childhood X-linked immunodeficiency, hyper IgM syndrome (HIGM1). IgE can however be detected in the ser

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Padayachee, M., R. J. Levinsky, C. Kinnon, et al. "Mapping of the X linked form of hyper IgM syndrome (HIGM1)." Journal of Medical Genetics 30, no. 3 (1993): 202–5. http://dx.doi.org/10.1136/jmg.30.3.202.

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7

Kroczek, Richard A., Daniel Graf, Duilio Brugnoni, et al. "Defective Expression of CD40 Ligand on T Cells Causes "X-Linked Immunodeficiency with Hyper-IgM (HIGM1)"." Immunological Reviews 138, no. 1 (1994): 39–59. http://dx.doi.org/10.1111/j.1600-065x.1994.tb00846.x.

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Padayachee, M., C. Feighery, A. Finn, et al. "Mapping of the x-linked form of hyper-IgM syndrome (HIGM1) to Xq26 by close linkage to HPRT." Genomics 14, no. 2 (1992): 551–53. http://dx.doi.org/10.1016/s0888-7543(05)80270-8.

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9

Hollenbaugh, D., L. H. Wu, H. D. Ochs, et al. "The random inactivation of the X chromosome carrying the defective gene responsible for X-linked hyper IgM syndrome (X-HIM) in female carriers of HIGM1." Journal of Clinical Investigation 94, no. 2 (1994): 616–22. http://dx.doi.org/10.1172/jci117377.

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10

Fontana, Stefania, Daniele Moratto, Surinder Mangal, et al. "Functional defects of dendritic cells in patients with CD40 deficiency." Blood 102, no. 12 (2003): 4099–106. http://dx.doi.org/10.1182/blood-2003-04-1244.

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Abstract We have recently identified 2 patients with a rare autosomal recessive form of hyper IgM disease, known as HIGM3, caused by mutations in the CD40 gene. These patients had opportunistic infections observed on X-linked hyper IgM syndrome (HIGM), suggesting that the CD40-CD40 ligand interaction is important for promoting T-cell-mediated immunity. To evaluate whether innate immunity signals may substitute CD154 for inducing the maturation of dendritic cells (DCs), we analyzed monocyte-derived DCs in these patients. Monocyte-derived DCs of HIGM3 subjects on ex vivo stimulation with tumor n

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Hoang, Ngoc H., Vera Strogolova, Jaramys J. Mosley, Rosemary A. Stuart, and Jonathan Hosler. "Hypoxia-inducible gene domain 1 proteins in yeast mitochondria protect against proton leak through complex IV." Journal of Biological Chemistry 294, no. 46 (2019): 17669–77. http://dx.doi.org/10.1074/jbc.ra119.010317.

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Hypoxia-inducible gene domain 1 (HIGD1) proteins are small integral membrane proteins, conserved from bacteria to humans, that associate with oxidative phosphorylation supercomplexes. Using yeast as a model organism, we have shown previously that its two HIGD1 proteins, Rcf1 and Rcf2, are required for the generation and maintenance of a normal membrane potential (ΔΨ) across the inner mitochondrial membrane (IMM). We postulated that the lower ΔΨ observed in the absence of the HIGD1 proteins may be due to decreased proton pumping by complex IV (CIV) or enhanced leak of protons across the IMM. He

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Wilson, Rebecca L., Weston Troja, Emily K. Sumser, Alec Maupin, Kristin Lampe, and Helen N. Jones. "Insulin-like growth factor 1 signaling in the placenta requires endothelial nitric oxide synthase to support trophoblast function and normal fetal growth." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 320, no. 5 (2021): R653—R662. http://dx.doi.org/10.1152/ajpregu.00250.2020.

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Currently, there is no effective treatment for placental dysfunction in utero. In a ligated mouse model of fetal growth restriction (FGR), nanoparticle-mediated human insulin-like 1 growth factor ( hIGF1) gene delivery (NP-Plac1-hIGF1) increased hIGF1 expression and maintained fetal growth. However, whether it can restore fetal growth remains to be determined. Using the endothelial nitric oxide synthase knockout (eNOS−/−) mouse model, a genetic model of FGR, we found that despite inducing expression of hIGF1 in the placentas treated with NP-Plac1-hIGF1 ( P = 0.0425), FGR did not resolve. This

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Di Leo, Vincenzo, Patrick J. Gleeson, Fabio Sallustio, et al. "Rifaximin as a Potential Treatment for IgA Nephropathy in a Humanized Mice Model." Journal of Personalized Medicine 11, no. 4 (2021): 309. http://dx.doi.org/10.3390/jpm11040309.

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IgA Nephropathy (IgAN) is the most common glomerulonephritis worldwide, characterized by the mesangial deposition of abnormally glycosylated IgA1 (Gd-IgA). The production of Gd-IgA occurs in mucose-associated lymphoid tissue (MALT). The microbiota plays a role in MALT modulation. Rifaximin (NORMIX®), a non-absorbable oral antibiotic, induces positive modulation of the gut microbiota, favoring the growth of bacteria beneficial to the host. Here, we evaluate the effect of rifaximin on a humanized mice model of IgAN (α1KI-CD89Tg). Methods: The α1KI-CD89Tg mice were treated by the vehicle (olive o

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Català-Moll, Francesc, Anna G. Ferreté-Bonastre, Tianlu Li, et al. "Activation-induced deaminase is critical for the establishment of DNA methylation patterns prior to the germinal center reaction." Nucleic Acids Research 49, no. 9 (2021): 5057–73. http://dx.doi.org/10.1093/nar/gkab322.

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Abstract Activation-induced deaminase (AID) initiates antibody diversification in germinal center B cells by deaminating cytosines, leading to somatic hypermutation and class-switch recombination. Loss-of-function mutations in AID lead to hyper-IgM syndrome type 2 (HIGM2), a rare human primary antibody deficiency. AID-mediated deamination has been proposed as leading to active demethylation of 5-methycytosines in the DNA, although evidence both supports and casts doubt on such a role. In this study, using whole-genome bisulfite sequencing of HIGM2 B cells, we investigated direct AID involvemen

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Bakhshpour, Monireh, Aykut Arif Topcu, Nilay Bereli, Huseyin Alkan, and Adil Denizli. "Poly(Hydroxyethyl Methacrylate) Immunoaffinity Cryogel Column for the Purification of Human Immunoglobulin M." Gels 6, no. 1 (2020): 4. http://dx.doi.org/10.3390/gels6010004.

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Human immunoglobulin M (hIgM) antibodies are considered as hopeful tools for diseases therapy. Therefore, chromatography approaches are used to purify hIgM with a single step. In this study, we prepared a poly(hydroxyethyl methacrylate) based immunoaffinity p(HEMA-I) cryogel column by using cyanamide to immobilize antihuman immunoglobulin on the p(HEMA) cryogel for purification of hIgM in aqueous solution and artificial human plasma. The characterization of the p(HEMA) cryogel column was performed by using a scanning electron microscope (SEM), micro-computerized tomography (µ-CT), Fourier tran

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Dong, Qiuting, Jinxia Zhao, Zhongqiang Yao, Xiangyuan Liu, and Huiying He. "A Case Report of X-Linked Hyperimmunoglobulin M Syndrome with Lipoma Arborescens of Knees." Case Reports in Medicine 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/5797232.

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The X-linked hyperimmunoglobulin M syndrome (HIGM), caused by mutations in the CD40LG gene, is a kind of primary immunodeficiency disease (PID). Patients with X-linked HIGM are susceptible to infection as well as autoimmune diseases. Lipoma arborescens (LA) is a rare benign tumor, of which the pathogenesis mechanism has not been clearly understood. We report a case of HIGM combined with LA in a 22-year-old male patient. A new deletion mutation of CD40LG gene was detected in this case. The possible relationship between HIGM and LA was also discussed.

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McLean, G. R., K. K. Miller, J. W. Schrader, and A. K. Junker. "Biased Immunoglobulin G (IgG) Subclass Production in a Case of Hyper-IgM Syndrome." Clinical Diagnostic Laboratory Immunology 11, no. 6 (2004): 1192–93. http://dx.doi.org/10.1128/cdli.11.6.1192-1193.2004.

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ABSTRACT Hyper-immunoglobulin M (IgM) syndrome (HIGM) is a rare heterogeneous primary immune deficiency. We describe a patient with HIGM characterized by skewed production of serum IgG subclasses and normal somatic hypermutation. This case may represent a subgroup of HIGM type 4 that is characterized by a biased switching to the V-region proximal constant regions.

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Sihombing, Martina Rentauli. "Clinical Aspect and Laboratory Test of Hyperimmunoglobulin M." Jurnal MedScientiae 3, no. 2 (2024): 260–69. http://dx.doi.org/10.36452/jmedscientiae.v3i2.3324.

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Hyperimmunoglobulin-M Syndrome (HIGM) is a set of symptomps due to primary immunodeficiency characterized by low levels of immunoglobulin G (IgG), immunoglobulin A (IgA), immunoglobulin E (IgE), and normal or increased levels of immunoglobulin M (IgM) or recurrent infections. HIGM syndrome was initially thought to be caused by genetic defects related to the X chromosome only, but along with advances in molecular technology in detecting genetic abnormalities, other autosomal-type defects were found. Genetic defects in HIGM Syndrome cause disruption of the maturation process of humoral immunity,

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Prakash, Prithivi Raaj, Gaurav Gupta, and Adarsh Aayilliath K. "Hyper IgM Syndromes: A Brief Review of the Pathogenesis, Clinical Features and Management." Journal of Clinical and Cellular Immunology 14, no. 4 (2023): 10. https://doi.org/10.35248/2155-9899.23.14.693.

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Primary Immuno Deficiency (PID) disorders are heterogeneous disorders of the innate or the adaptive immune system, leading to recurrent infections that can also predispose to autoimmune diseases and malignancies. Hyper IgM Syndromes (HIGM) are rare disorders characterized by defective Class Switch Recombination (CSR) and/or Somatic Hypermutation (SHM) resulting in decreased levels of IgG, IgE and IgA antibodies and normal or elevated IgM levels. Various genetic defects have been identified to cause HIGM syndromes. These include intrinsic B cell defects or defects in the interaction between T a

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DERRIDA, JACQUES. "Le toucherTouch/to touch him1." Paragraph 16, no. 2 (1993): 122–57. http://dx.doi.org/10.3366/para.1993.0004.

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Chemouny, Jonathan M., Patrick J. Gleeson, Lilia Abbad, et al. "Modulation of the microbiota by oral antibiotics treats immunoglobulin A nephropathy in humanized mice." Nephrology Dialysis Transplantation 34, no. 7 (2018): 1135–44. http://dx.doi.org/10.1093/ndt/gfy323.

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Abstract Background Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. IgA is mainly produced by the gut-associated lymphoid tissue (GALT). Both experimental and clinical data suggest a role of the gut microbiota in this disease. We aimed to determine if an intervention targeting the gut microbiota could impact the development of disease in a humanized mouse model of IgAN, the α1KI-CD89Tg mice. Methods Four- and 12-week old mice were divided into two groups to receive either antibiotics or vehicle control. Faecal bacterial load and proteinuria were qua

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Keenan, Thomas D., Suresh Radhakrishnan, Michael Bell, Michael Barry, and Larry R. Pease. "Retargeting IgM Antibodies with Different Specificities to a Common Cell Type Reveals Shared Mechanisms Regulating Cellular Activation (91.12)." Journal of Immunology 182, no. 1_Supplement (2009): 91.12. http://dx.doi.org/10.4049/jimmunol.182.supp.91.12.

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Abstract IgM antibodies, as multivalent ligands, have the capacity to activate cells differentially by cross-linking targeted cell surface signaling molecules. For example, hIgM12 (B7DC Xab) activates dendritic cells (DCs), leading to potent immunomodulation, while hIgM22 binds glial cells and causes remyelination in mouse models of multiple sclerosis. Both antibodies activate common signaling intermediates in their respective cellular targets suggesting a common mechanism of action. Elucidation of these shared mechanisms became possible by targeting both antibodies to a common cell type. Our

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Corey, Daniel, and Irving L. Weissman. "Super Cross-Presentation of Tumor Antigens to Elicit Anti-Lymphoma Immunity By Synthetic Design of an Anti-Phosphatidylserine Bridge Protein." Blood 128, no. 22 (2016): 1844. http://dx.doi.org/10.1182/blood.v128.22.1844.1844.

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Abstract Cell loss by apoptosis is a common feature in tumors. Dying tumor cells induce immune tolerance within the tumor microenvironment largely through highly conserved homeostatic clearance programs that restore tissue immune homeostasis and contribute to the formation of an immunosuppressive niche. The translocation of phosphatidylserine (PS) on cellular membranes, during the initial phases of apoptosis, functions as a recognition and removal signal that limits the immunogenicity of cell death. We examined whether altering clearance of dying cancer cells to elicit inflammatory turnover po

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Crasson, Aurèle, Jean-Louis Lebrave, Jérémy Pedrazzi, and Laurent Alonso. "Le toucher Touch/to touch him1." Genesis, no. 55 (December 1, 2022): 1–200. http://dx.doi.org/10.4000/genesis.7747.

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Takeda, Tadayuki, Keiko Ogino, Etsuko Matsui, et al. "A Fission Yeast Gene,him1+/dfp1+, Encoding a Regulatory Subunit for Hsk1 Kinase, Plays Essential Roles in S-Phase Initiation as Well as in S-Phase Checkpoint Control and Recovery from DNA Damage." Molecular and Cellular Biology 19, no. 8 (1999): 5535–47. http://dx.doi.org/10.1128/mcb.19.8.5535.

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ABSTRACT Saccharomyces cerevisiae CDC7 encodes a serine/threonine kinase required for G1/S transition, and its related kinases are present in fission yeast as well as in higher eukaryotes, including humans. Kinase activity of Cdc7 protein depends on the regulatory subunit, Dbf4, which also interacts with replication origins. We have identified him1+ from two-hybrid screening with Hsk1, a fission yeast homologue of Cdc7 kinase, and showed that it encodes a regulatory subunit of Hsk1. Him1, identical to Dfp1, previously identified as an associated molecule of Hsk1, binds to Hsk1 and stimulates i

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Braster, Rens, Marijn Bögels, Hreinn Benonisson та ін. "Afucosylated IgG Targets FcγRIV for Enhanced Tumor Therapy in Mice". Cancers 13, № 10 (2021): 2372. http://dx.doi.org/10.3390/cancers13102372.

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Promising strategies for maximizing IgG effector functions rely on the introduction of natural and non-immunogenic modifications. The Fc domain of IgG antibodies contains an N-linked oligosaccharide at position 297. Human IgG antibodies lacking the core fucose in this glycan have enhanced binding to human (FcγR) IIIa/b, resulting in enhanced antibody dependent cell cytotoxicity and phagocytosis through these receptors. However, it is not yet clear if glycan-enhancing modifications of human IgG translate into more effective treatment in mouse models. We generated humanized hIgG1-TA99 antibodies

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Subauste, Carlos S., Matthew Wessendarp, Ricardo U. Sorensen, and Lily E. Leiva. "CD40-CD40 Ligand Interaction Is Central to Cell-Mediated Immunity Against Toxoplasma gondii: Patients with Hyper IgM Syndrome Have a Defective Type 1 Immune Response That Can Be Restored by Soluble CD40 Ligand Trimer." Journal of Immunology 162, no. 11 (1999): 6690–700. http://dx.doi.org/10.4049/jimmunol.162.11.6690.

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Abstract Cell-mediated immunity that results in IL-12/IFN-γ production is essential to control infections by intracellular organisms. Studies in animal models revealed contrasting results in regard to the importance of CD40-CD40 ligand (CD40L) signaling for induction of a type 1 cytokine response against these pathogens. We demonstrate that CD40-CD40L interaction in humans is critical for generation of the IL-12/IFN-γ immune response against Toxoplasma gondii. Infection of monocytes with T. gondii resulted in up-regulation of CD40. CD40-CD40L signaling was required for optimal T cell productio

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Baeker, T. R., and T. L. Rothstein. "Proliferation of human malignant lymphocytes induced by anti-IgM independent of B cell growth factor." Journal of Immunology 134, no. 5 (1985): 3532–38. http://dx.doi.org/10.4049/jimmunol.134.5.3532.

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Abstract Human malignant B lymphocytes were identified that proliferate in response to small doses of anti-immunoglobulin. Proliferation was induced by monoclonal mouse anti-HIgM, polyclonal goat anti-HIgM, and F(ab')2 fragments thereof, in vitro, and was not accompanied by immunoglobulin secretion. Proliferation was found to be unaffected by T cell depletion and was not enhanced by supplementation with B cell growth factor. Culture fluids from unstimulated malignant lymphocytes as well as from malignant lymphocytes stimulated with anti-HIgM contained no measurable B cell growth factor activit

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Sullivan, Kathleen E. "IMMUNOHISTOLOGIC ANALYSIS OF INEFFECTIVE CD40-CD40 LIGAND INTERACTION IN LYMPHOID TISSUES FROM PATIENTS WITH X-LINKED IMMUNODEFICIENCY WITH HYPER-IgM." Pediatrics 98, no. 2 (1996): 350. http://dx.doi.org/10.1542/peds.98.2.350.

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The functional development of B cell follicles and follicular dendritic cells require CD40-CD40 ligand interactions. Both of these abnormalities probably contribute to the immunodeficiency in HIGMX-1.

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WEISS, S., F. ZENG, and V. BONAGURA. "841 Hyper-IgM syndrome (HIgMs): A B-cell defect." Journal of Allergy and Clinical Immunology 97, no. 1 (1996): 393. http://dx.doi.org/10.1016/s0091-6749(96)81059-1.

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Willoughby, Jane E., Lang Dou, Sabyasachi Bhattacharya, et al. "Impact of isotype on the mechanism of action of agonist anti-OX40 antibodies in cancer: implications for therapeutic combinations." Journal for ImmunoTherapy of Cancer 12, no. 7 (2024): e008677. http://dx.doi.org/10.1136/jitc-2023-008677.

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BackgroundOX40 has been widely studied as a target for immunotherapy with agonist antibodies taken forward into clinical trials for cancer where they are yet to show substantial efficacy. Here, we investigated potential mechanisms of action of anti-mouse (m) OX40 and anti-human (h) OX40 antibodies, including a clinically relevant monoclonal antibody (mAb) (GSK3174998) and evaluated how isotype can alter those mechanisms with the aim to develop improved antibodies for use in rational combination treatments for cancer.MethodsAnti-mOX40 and anti-hOX40 mAbs were evaluated in a number of in vivo mo

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Chang, Chih-Ching, Janet R. Gilsdorf, Victor J. DiRita, and Carl F. Marrs. "Identification and Genetic Characterization ofHaemophilus influenzae Genetic Island 1." Infection and Immunity 68, no. 5 (2000): 2630–37. http://dx.doi.org/10.1128/iai.68.5.2630-2637.2000.

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ABSTRACT The type b capsule of pathogenic Haemophilus influenzaeis a critical factor for H. influenzae survival in the blood and the establishment of invasive infections. Other pathogenic factors associated with type b strains may also play a role in invasion and sustained bacteremia, leading to the seeding of deep tissues. The gene encoding haemocin is the only noncapsular gene found to be specific to type b strains until now. Here we report the discovery of an approximately 16-kb genetic locus, HiGI1, that is present primarily in type b strains. Pulsed-field gel electrophoresis and Southern

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Chen, Xinhai, Miaomiao Shi, Xin Tong, et al. "Glycosylation-dependent opsonophagocytic activity of staphylococcal protein A antibodies." Proceedings of the National Academy of Sciences 117, no. 37 (2020): 22992–3000. http://dx.doi.org/10.1073/pnas.2003621117.

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Antibodies may bind to bacterial pathogens or their toxins to control infections, and their effector activity is mediated through the recruitment of complement component C1q or the engagement with Fcγ receptors (FcγRs). For bacterial pathogens that rely on a single toxin to cause disease, immunity correlates with toxin neutralization. Most other bacterial pathogens, including Staphylococcus aureus, secrete numerous toxins and evolved multiple mechanisms to escape opsonization and complement killing. Several vaccine candidates targeting defined surface antigens of S. aureus have failed to meet

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Tipton, Thomas R. W., Ali Roghanian, Robert J. Oldham, et al. "Antigenic modulation limits the effector cell mechanisms employed by type I anti-CD20 monoclonal antibodies." Blood 125, no. 12 (2015): 1901–9. http://dx.doi.org/10.1182/blood-2014-07-588376.

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Key Points Antigenic modulation significantly impacts natural killer cell and macrophage ability to mediate Fc γ receptor-dependent killing. hIgG1 mAbs are unable to elicit natural killer–mediated ADCC in the mouse, supporting ADCP as the dominant effector mechanism.

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Wang, Q. Daniel. "X-Ray Observations of the Hot Intergalactic Medium." Symposium - International Astronomical Union 188 (1998): 193–96. http://dx.doi.org/10.1017/s0074180900114743.

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A definite prediction from recent N-body/hydro simulations of the structure formation of the universe is the presence of a diffuse hot intergalactic medium (HIGM; e.g., Ostriker & Cen 1996). The filamentary structure of the today's universe, as seen in various galaxies surveys, is thought to be a result of the gravitational collapse of materials from a more-or-less uniform and isotropic early universe. During the collapse, shock-heating can naturally raise gas temperature to a range of 105 – 107 K. Feedbacks from stars may also be an important heating source and may chemically enrich the H

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Chen, Xiangjun, Xiaolin Sun, Wei Yang, et al. "An autoimmune disease variant of IgG1 modulates B cell activation and differentiation." Science 362, no. 6415 (2018): 700–705. http://dx.doi.org/10.1126/science.aap9310.

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The maintenance of autoreactive B cells in a quiescent state is crucial for preventing autoimmunity. Here we identify a variant of human immunoglobulin G1 (IgG1) with a Gly396→Arg substitution (hIgG1-G396R), which positively correlates with systemic lupus erythematosus. In induced lupus models, murine homolog Gly390→Arg (G390R) knockin mice generate excessive numbers of plasma cells, leading to a burst of broad-spectrum autoantibodies. This enhanced production of antibodies is also observed in hapten-immunized G390R mice, as well as in influenza-vaccinated human G396R homozygous carriers. This

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Razanajaona, D., C. van Kooten, S. Lebecque, et al. "Somatic mutations in human Ig variable genes correlate with a partially functional CD40-ligand in the X-linked hyper-IgM syndrome." Journal of Immunology 157, no. 4 (1996): 1492–98. http://dx.doi.org/10.4049/jimmunol.157.4.1492.

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Abstract X-linked hyper-IgM (HIGM-1) syndrome is a rare disorder resulting from mutations in the CD40-ligand (CD40L) gene. This defect is associated with normal or elevated serum levels of IgM, and with low to undetectable levels of serum IgG, IgA, and IgE. We analyzed the somatic mutation status in Ig V genes from three unrelated HIGM-1 patients by reverse-transcription PCR and sequence analysis. Two patients (B.S. and P.S.) expressed unmutated VH6 genes. In contrast, one patient (A.T.) was found to express mutated VH6 genes. Whether the presence of somatic mutations in this patient was relat

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Toropainen, Maija, Leena Saarinen, Gestur Vidarsson, and Helena Käyhty. "Protection by Meningococcal Outer Membrane Protein PorA-Specific Antibodies and a Serogroup B Capsular Polysaccharide-Specific Antibody in Complement-Sufficient and C6-Deficient Infant Rats." Infection and Immunity 74, no. 5 (2006): 2803–8. http://dx.doi.org/10.1128/iai.74.5.2803-2808.2006.

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ABSTRACT The relative contributions of antibody-induced complement-mediated bacterial lysis and antibody/complement-mediated phagocytosis to host immunity against meningococcal infections are currently unclear. Further, the in vivo effector functions of antibodies may vary depending on their specificity and Fc heavy-chain isotype. In this study, a mouse immunoglobulin G2a (mIgG2a) monoclonal antibody (MN12H2) to meningococcal outer membrane protein PorA (P1.16), its human IgG subclass derivatives (hIgG1 to hIgG4), and an mIgG2a monoclonal antibody (Nmb735) to serogroup B capsular polysaccharid

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Iurian, Sorin Ioan, Laszlo Marodi, and Capucine Picard. "Peculiar hyper-IgM syndrome. Case report / Sindrom hiper-IgM atipic. Prezentare de caz." Revista Romana de Medicina de Laborator 23, no. 3 (2015): 341–45. http://dx.doi.org/10.1515/rrlm-2015-0027.

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AbstractWe report a male infant diagnosed at the age of 10 months with hyper-IgM syndrome (HIGM) in context of severe infections caused by Streptococcus pneumoniae, Staphylococcus aureus and Candida albicans. In patient’s outcome, in spite of immunoglobulin therapy, he continues presenting bilateral suppurative otitis media due to both Candida and penicillin-resistant pneumococcus and forearm abscess caused by Staphylococcus aureus. The infant developed bilateral cataracts, chronic hepatitis and comminuted fracture secondary to bone demineralization. The patient didn’t develop opportunistic in

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Gallo, Vera, Emilia Cirillo, Rosaria Prencipe, et al. "Clinical, Immunological, and Functional Characterization of Six Patients with Very High IgM Levels." Journal of Clinical Medicine 9, no. 3 (2020): 818. http://dx.doi.org/10.3390/jcm9030818.

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Very high IgM levels represent the hallmark of hyper IgM (HIGM) syndromes, a group of primary immunodeficiencies (PIDs) characterized by susceptibility to infections and malignancies. Other PIDs not fulfilling the diagnostic criteria for HIGM syndromes can also be characterized by high IgM levels and susceptibility to malignancies. The aim of this study is to characterize clinical phenotype, immune impairment, and pathogenic mechanism in six patients with very high IgM levels in whom classical HIGM syndromes were ruled out. The immunological analysis included extended B-cell immunophenotyping,

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Hartley, Andrew M., Brigitte Meunier, Nikos Pinotsis, and Amandine Maréchal. "Rcf2 revealed in cryo-EM structures of hypoxic isoforms of mature mitochondrial III-IV supercomplexes." Proceedings of the National Academy of Sciences 117, no. 17 (2020): 9329–37. http://dx.doi.org/10.1073/pnas.1920612117.

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The organization of the mitochondrial electron transport chain proteins into supercomplexes (SCs) is now undisputed; however, their assembly process, or the role of differential expression isoforms, remain to be determined. In Saccharomyces cerevisiae, cytochrome c oxidase (CIV) forms SCs of varying stoichiometry with cytochrome bc1 (CIII). Recent studies have revealed, in normoxic growth conditions, an interface made exclusively by Cox5A, the only yeast respiratory protein that exists as one of two isoforms depending on oxygen levels. Here we present the cryo-EM structures of the III2-IV1 and

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Lee, Wen-I., Troy R. Torgerson, Michael J. Schumacher, Leman Yel, Qili Zhu, and Hans D. Ochs. "Molecular analysis of a large cohort of patients with the hyper immunoglobulin M (IgM) syndrome." Blood 105, no. 5 (2005): 1881–90. http://dx.doi.org/10.1182/blood-2003-12-4420.

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AbstractThe hyper immunoglobulin M (IgM) syndrome (HIGM), characterized by recurrent infections, low serum IgG and IgA, normal or elevated IgM, and defective class switch recombination and somatic hypermutation, is a heterogenous disorder with at least 5 distinct molecular defects, including mutations of the genes coding for the CD40 ligand (CD40L) and IKK-gamma (NEMO) genes, both X-linked; and mutations of CD40, activation-induced cytidine deaminase (AICDA), and uracil-DNA glycosylase (UNG), associated with autosomal recessive HIGM syndromes. To investigate the molecular basis of HIGM, we det

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Jiang, Ning, Wei Chen, Prithiviraj Jothikumar та ін. "Effects of anchor structure and glycosylation of Fcγ receptor III on ligand binding affinity". Molecular Biology of the Cell 27, № 22 (2016): 3449–58. http://dx.doi.org/10.1091/mbc.e16-06-0470.

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Isoforms of the Fcγ receptor III (FcγRIII or CD16) are cell surface receptors for the Fc portion of IgG and important regulators of humoral immune responses. Different ligand binding kinetics of FcγRIII isoforms are obtained in three dimensions by surface plasmon resonance and in two dimensions by a micropipette adhesion frequency assay. We show that the anchor structure of CD16 isoforms isolated from the cell membrane affects their binding affinities in a ligand-specific manner. Changing the receptor anchor structure from full to partial to none decreases the ligand binding affinity for human

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Maslova, N. N., and A. Ye Iusov. "ANALYSIS OF THE RELATIONSHIP DIAGNOSED MILD COGNITIVE IMPAIRMENT IN ELDERLY AND SENILE PATIENTS WITH CERTAIN FEATURES OF MEDICAL HISTORY AND DEPRESSION." Bulletin of Siberian Medicine 12, no. 5 (2013): 46–50. http://dx.doi.org/10.20538/1682-0363-2013-5-46-50.

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Are defined frequency of mild cognitive impairment (MCI) at patients of advanced and senile age with chronic ischemia of a brain (HIGM) in comparison with frequency of existence of a depression, an education level and the place of residence and their interrelation. 100 patients with HIGM 2 age групп: 1 – advanced age (from 60 to 74 years – 48 people), 2 – senile age (from 75 to 89 years – 52 persons) are surveyed. In research didn't join: patients with Alzheimer's disease and other forms of a dementias. Diagnostics of UKN it was carried out by means of a short scale of an assessment of the men

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Couvidou, Adèle, Mathieu Wald, Catherine Angénieux, et al. "Anti-HLA-I IgG Subclass Influences Antibody-Mediated Platelet Activation in the Context of Platelet Transfusion Refractoriness." Blood 144, Supplement 1 (2024): 2642. https://doi.org/10.1182/blood-2024-197921.

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Background: Patients requiring extensive platelet transfusion support are prone to platelet transfusion refractoriness (PTR), a therapeutic failure of platelet transfusion due to the rapid clearance of transfused platelets from the circulation. PTR can be attributed to the presence of allogeneic anti-HLA class I (HLA-I) antibodies (Abs) within the recipient's circulation. This leads to the rapid elimination of transfused platelets through mechanism that remains poorly understood. Strikingly, not all patients with anti-HLA-I Abs develop PTR upon platelet transfusions raising the question whethe

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Hubbard, Nicholas, David Hagin, Karen Sommer, et al. "Targeted gene editing restores regulated CD40L function in X-linked hyper-IgM syndrome." Blood 127, no. 21 (2016): 2513–22. http://dx.doi.org/10.1182/blood-2015-11-683235.

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Key PointsThe CD40LG locus can be specifically targeted and repaired in primary human T cells by insertion of a spliced CD40LG complementary DNA. Gene editing restores regulated CD40L expression in X-HIGM T cells, reconstituting B-cell immunoglobulin class switching.

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Hubbard, Nicholas Wesley, David Hagin, Karen Sommer, et al. "Targeted Gene Editing Restores Regulated CD40L Expression and Function in X-HIGM T cells." Journal of Immunology 196, no. 1_Supplement (2016): 214.28. http://dx.doi.org/10.4049/jimmunol.196.supp.214.28.

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Abstract Loss of CD40L expression or function results in X-Linked Hyper-IgM Syndrome (X-HIGM), characterized by recurrent infections due to impaired immunoglobulin class-switching and somatic hypermutation. Previous attempts using retroviral gene transfer to correct murine CD40L expression restored immune function; however, treated mice developed lymphoproliferative disease, likely due to viral-promoter dependent constitutive CD40L expression. These observations highlight the importance of preserving endogenous gene regulation in order to safely correct this disorder. Here we report efficient,

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Ramesh, Narayanaswamy, Tomohiro Morio, Ramsay Fuleihan, et al. "CD40—CD40 ligand (CD40L) interactions and X-linked hyperIgM syndrome (HIGMX-1)." Clinical Immunology and Immunopathology 76, no. 3 (1995): S208—S213. http://dx.doi.org/10.1016/s0090-1229(95)90252-x.

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Wilson, Jacqueline Z. "Adolescent resistance narratives in a satirical schoolyard: the case ofSummer Heights High1." Journal of Australian Studies 33, no. 3 (2009): 305–16. http://dx.doi.org/10.1080/14443050903079698.

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Gosselin, E. J., K. Wardwell, D. R. Gosselin, N. Alter, J. L. Fisher, and P. M. Guyre. "Enhanced antigen presentation using human Fc gamma receptor (monocyte/macrophage)-specific immunogens." Journal of Immunology 149, no. 11 (1992): 3477–81. http://dx.doi.org/10.4049/jimmunol.149.11.3477.

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Abstract A major new challenge for vaccine development is to target APC such as monocytes and macrophages for efficient Ag processing and presentation. It has been shown that Fc gamma R-mediated uptake of Ag-antibody complexes can enhance Ag presentation by myeloid cells at least 100-fold, and directing Ag to Fc gamma R in mice brings about a substantial increase in the effectiveness of immunization while eliminating the requirement for adjuvant. It has not been determined which of the three subclasses of human Fc gamma R on myeloid cells (Fc gamma RI, Fc gamma RII, or Fc gamma RIII) function

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