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Academic literature on the topic 'Immunoglobin; Blood cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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Journal articles on the topic "Immunoglobin; Blood cells"

Tan, Peng H., John B. Yates, Shao-An Xue, Cliburn Chan, William J. Jordan, Jennifer E. Harper, Martin P. Watson, et al. "Creation of tolerogenic human dendritic cells via intracellular CTLA4: a novel strategy with potential in clinical immunosuppression." Blood 106, no. 9 (November 1, 2005): 2936–43. http://dx.doi.org/10.1182/blood-2005-05-1826.

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AbstractActivation of T lymphocytes requires the recognition of peptide–major histocompatibility complexes (MHCs) and costimulatory signals provided by antigen-presenting cells (APCs). It has been shown that T-cell activation without costimulation can lead to anergy. In this study, we developed a novel strategy to inhibit expression of B7 molecules (CD80/86) by transfecting APCs with a gene construct encoding a modified cytotoxic T lymphocyte antigen 4 (CTLA4) molecule (CTLA4-KDEL) that is targeted to the endoplasmic reticulum (ER). APCs expressing this construct failed to express CD80/86 on their surface, were unable to stimulate allogeneic and peptide-specific T-cell responses, and induced antigen-specific anergy of the responding T cells. Cells expressing CTLA4-KDEL do not up-regulate the indoleamine 2, 3-dioxygenase enzyme, unlike cells treated with soluble CTLA4-immunoglobin (Ig). This gene-based strategy to knock out surface receptors is an attractive alternative to using immature dendritic cells for preventing transplant rejection and treating of autoimmune diseases.

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Kay, NE, and RT Perri. "Evidence that large granular lymphocytes from B-CLL patients with hypogammaglobulinemia down-regulate B-cell immunoglobulin synthesis [published erratum appears in Blood 1989 Jun;73(8):2232]." Blood 73, no. 4 (March 1, 1989): 1016–19. http://dx.doi.org/10.1182/blood.v73.4.1016.bloodjournal7341016.

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B-chronic lymphocytic leukemia (CLL) patients frequently suffer from moderate to severe hypogammaglobulinemia. This complication is a serious cause of morbidity and mortality in this disorder. There is recent evidence that natural killer (NK) cells modulate B-cell immunoglobin (Ig) synthesis/secretion. The authors therefore evaluated the circulating NK cells from B-CLL patients on their ability to regulate mitogen-induced B-cell Ig synthesis. Blood, NK cells (CD16+, CD3-) from three B-CLL patients with hypogammaglobulinemia were able to clearly down-regulate the pokeweed mitogen (PWM)-induced-B-cell Ig secretion. In contrast, CD16+, CD3- cells from age-sex-matched controls or B-CLL patients with normal Ig were either nonregulatory or enhanced mitogen-induced B-cell Ig secretion. An alternative explanation for hypogammaglobulinemia in B-CLL patients is the immunomodulation of B- cell Ig production/secretion by CD16+, CD3- blood cells.

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Abstract B-chronic lymphocytic leukemia (CLL) patients frequently suffer from moderate to severe hypogammaglobulinemia. This complication is a serious cause of morbidity and mortality in this disorder. There is recent evidence that natural killer (NK) cells modulate B-cell immunoglobin (Ig) synthesis/secretion. The authors therefore evaluated the circulating NK cells from B-CLL patients on their ability to regulate mitogen-induced B-cell Ig synthesis. Blood, NK cells (CD16+, CD3-) from three B-CLL patients with hypogammaglobulinemia were able to clearly down-regulate the pokeweed mitogen (PWM)-induced-B-cell Ig secretion. In contrast, CD16+, CD3- cells from age-sex-matched controls or B-CLL patients with normal Ig were either nonregulatory or enhanced mitogen-induced B-cell Ig secretion. An alternative explanation for hypogammaglobulinemia in B-CLL patients is the immunomodulation of B- cell Ig production/secretion by CD16+, CD3- blood cells.

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Karkhanis, Vrajesh, Warren Fiskus, Christopher Peter Mill, Abhishek Maiti, Bernardo H. Lara, James V. Maher, Isean Bhalla, et al. "Efficacy of Targeted Therapy in Novel Pre-Clinical in Vitro and In Vivo Models of Richter Transformation-Diffuse Large B-Cell Lymphoma (RT-DLBCL)." Blood 134, Supplement_1 (November 13, 2019): 3961. http://dx.doi.org/10.1182/blood-2019-132041.

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Richter Transformation (RT) is defined as the development of aggressive DLBCL (mostly ABC-type) in up to ~15% of patients with antecedent or concurrent diagnosis of CLL. Based on the comparison of immunoglobin gene rearrangements, approximately 80% of RT-DLBCL arise due to a direct clonal evolution of the underlying CLL clone, i.e., clonally related (CLR) RT-DLBCL, which exhibit poor median survival (MS) of one year. Approximately 20% of RT-DLBCLs are clonally unrelated (CUR) to the underlying CLL, arising most likely due to branched clonal evolution from a common pre-CLL progenitor. CUR RT-DLBCLs exhibit a better MS of 5 years. Although chemo-immunotherapy and treatment with the Bruton's tyrosine kinase (BTK) inhibitor ibrutinib or anti-apoptotic BCL2 inhibitor venetoclax can induce remissions, they fail to induce prolonged disease-free survival in RT-DLBCL. Majority of patients relapse with therapy-refractory disease. Lack of availability of in vitro cultured RT-DLBCL cells or PD xenograft models has prevented pre-clinical testing and development of novel targeted agents against RT-DLBCL. Here, we report the establishment of 3 patient-derived xenograft (PDX) models of RT-DLBCL. Based on immunoglobulin heavy chain (IGH) clonality testing by NGS, the RT-DLBCL RT17 was CLR, RT15 was CUR and RT5 was of indeterminate clonality. The PDXs were generated by tail-vein infusion and engraftment of luciferase-transduced CD19+ RT-DLBCL cells in NSG mice. The RT-DLBCL PDXs grew in the bone marrow and spleen, causing marked splenomegaly, requiring euthanasia 4 to 6 weeks after engraftment. All three RT-DLBCL PDX cells were EBV-negative by genomic and EBNA2 protein expression analyses. NextGen DNA sequencing of RT17, RT15, and RT5 cells showed large numbers of genetic mutations, including mutations in TP53, ATM, NOTCH2, TET2 and MLL3 genes with a high variant allelic frequencies. Array-CGH showed DNA copy gains or losses in multiple chromosomes, including 3, 8, 9, 11, 12, 17 and 18. A 5'-MYC amplification was detected by FISH analysis in RT5 DLBCL cells. ATAC-Seq showed increased signal intensity representing increased chromatin accessibility in the RT-DLBCL cells compared to CD34+ normal progenitors. High peak numbers were detected in specific loci, including TCF4, PAX5, IRF4, MYB, MYC, BCL2L1 and BCL-2. Anti-H3K27Ac ChIP-Seq analysis showed increased average, normalized read-densities at super-enhancers/enhancers (SEs/Es), including those of TCF4, PAX5, IRF4, BCL2 (RT17 and RT15) and MYC (RT5). Western analyses showed that all three RT-DLBCL PDX cells expressed TCF4, c-Myc, and BRD4, with highest expression in RT5 cells. Accordingly, RT5 cells were more sensitive than cells RT17 and RT15 cells to the BET protein inhibitor (BETi) OTX015-induced apoptosis. This was associated with greater, OTX015-mediated, depletion of c-Myc in RT5 cells. RT17 and RT15 expressed high levels of BCL2, Bcl-xL and MCL1, whereas RT5 lacked BCL2 expression. Consistent with this, RT17 and RT15 cells were significantly more sensitive than RT5 cells to venetoclax-induced apoptosis (p < 0.01). RT17 and RT15, but not RT5 cells, expressed NFkB2 (p52), consistent with activation of non-canonical NFkB signaling. This was associated with resistance of RT17 and RT15 cells to ibrutinib-induced apoptosis (p < 0.001). However, co-treatment with OTX015 and ibrutinib or venetoclax induced synergistic lethality in all RT-DLBCL cells (combination indices < 1.0). BET-PROTAC ARV-825 and ARV-771 treatment depleted BRD4, leading to marked reduction in c-Myc levels and apoptosis of all RT-DLBCL cells. Treatment with the ATP-competitive, CDK9 inhibitor NVP2 also dose-dependently induced apoptosis in RT-DLBCL cells associated with depletion of c-Myc, Bcl-xL, and MCL1 protein levels. These findings highlight the activity and support further in vitro and in vivo evaluation of BETi, BET-PROTAC or CDK9i-based combinations with ibrutinib or venetoclax against genetically-profiled RT-DLBCL cells that are clonally-related or clonally-unrelated to the antecedent CLL. Disclosures Maiti: Celgene: Other: research funding. Bhalla:Beta Cat Pharmaceuticals: Consultancy. Khoury:Angle: Research Funding; Stemline Therapeutics: Research Funding; Kiromic: Research Funding.

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Wang, Jing, Shuang Geng, Yuping Zhong, Mingyi Chen, Wenming Wang, Yuhong Pang, Jiajia Zhang, Yuanyuan Liu, Yanyi Huang, and Hongmei Jing. "Detection of Circulating Plasma Cells in Multiple Myeloma with Extramedullary Plasmacytoma." Blood 126, no. 23 (December 3, 2015): 5328. http://dx.doi.org/10.1182/blood.v126.23.5328.5328.

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Abstract Objective: To detect the circulating plasma cells (cPCs) in patients of multiple myeloma (MM) with or withoutextramedullary plasmacytoma (EMP). Methods: The 21 patients of MM samples were collected from April 2014 to April 2015. There were 12 males, 9 females, with a median age of 60 (49 to 76 years old). Peripheral blood and bone marrow were examined before treatment or after EMP. Multi parameter flow cytometry (MFC) was used to analyze abnormal plasma cells (tumor cells) in samples of bone marrow and CD138 MACS positive sorting peripheral blood. The antibodies used in the flow cytometry were CD38-APC, CD138-PE, CD81-PE-Cy7, CD45-PacBlue, CD19-Percp-Cy5.5, CD56-mCherry-PE-ef610, CD117-AmCyan, CD16, Zombie-APC-Cy7. Results: In these 21 patients, he ratio of sex is 1.33:1, the median age is 60 (49-76). The immunoglobin type is as follows: IgG κ 7 cases, IgG λ 5 cases, IgG 2 cases, IgA κ 3 cases, IgA λ 2 cases, λ light chain 1 cases. The morphology of bone marrow aspiration showed more than 15% plasma cells and abnormal plasma cells can be seen in bone marrow in cytometry. 9 of 21 patients diagnosed MM with EMP, 2 of them find EMP when initial diagnosis and 7 of them find EMP in the course of disease (6 months to 8 years). The sites of the EMP included head, jaw, chest wall, side of the rib, the soft tissue of the sacral region and the vertebral body and all patients had bone involvement. In 17 patients with complete clinical data, bone marrow and peripheral blood specimens, the cPCs negative rate was 87.5%(7/8) in EMP negative patients, while the cPCs positive rate was 66.7% (6/9) in EMP positive patients, the difference among groups was statistically significant (chi square values: 5.13, p = 0.024). Conclusion: MFC has been widely used in diagnosis and minimal residual disease surveillance of MM, here we established the detection method of cPCs in MM patients, and it is valuable for clinical diagnosis and prognosis judgment. Disclosures No relevant conflicts of interest to declare.

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Gilbreath, Tyler, Samantha Swenson, and Shannon M. Buckley. "Role of Ubiquitin E3 Ligase UBR5 in B-Cell Development and Lymphoma." Blood 134, Supplement_1 (November 13, 2019): 2794. http://dx.doi.org/10.1182/blood-2019-128747.

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Mantle Cell Lymphoma (MCL) is a non-Hodgkin's lymphoma (NHL) that typically affects older adults. In MCL, there is uncontrolled growth of B cells within the mantle zone of lymph node and spleen germinal centers. The vast majority of MCL cases have a translocation of chromosome 11 and 14 which juxtaposes the cyclin D1 gene, CCND1, with the immunoglobin heavy chain gene promoter (Eµ) and leads to the overexpression of CCND1. This translocation of CCND1 is not enough to cause MCL by itself and additional mutations are needed for MCL to develop. Although MCL only represents ~5% of NHL patients, it has the poorest survival rate among NHL sub-types due to a lack of successful therapeutic treatments. As such, it is important to identify potential targets for treatment. Recently published data shows that in 18% of all MCL patients have a mutation in the gene encoding the E3 ubiquitin ligase, UBR5. UBR5 is part of the ubiquitin proteasome system, a degradation/recycling pathway in which proteins are tagged with a ubiquitin protein and degraded by the proteasome. Of the identified UBR5 mutations, over 60% of the mutations are truncations at the carboxy terminus that cut off the cysteine residue linked to ubiquitin transfer in exon 59 suggesting a catalytic dead mutant protein is produced. Interestingly, UBR5HECT mutations are specific to MCL and are not found in other sub-types of NHL. By studying UBR5, we can determine the role of UBR5 mutations in MCL, elucidate molecular mechanism of UBR5 in B cell development, and identify potential therapeutic targets. In order to study the role of UBR5 in B cell development and MCL, we generated a conditional mouse model targeting exon 58 similar to mutations in MCL patients and crossed the mice with Mb1CRE/WT mice to delete exon 58 specifically in B cells at the pro-pre B cell stage of B cell development. Mb1CRE/WT; Ubr5fl/fl mice shows that mice lacking the carboxy terminus of UBR5 have a block in B cell differentiation at the mature B cell IgM+ IgD+ stage within the spleen. Mb1CRE/WT; Ubr5fl/fl mice showed a marked decrease of mature IgM+ IgD+ B cells in the BM and spleen. Specifically, within the spleen, Mb1CRE/WT; Ubr5fl/fl mice produce abnormal follicular B cells (higher IgM and CD23 expression and lower IgD and CD22 expression) and significant reductions in marginal zone B cells, plasma cells, size of germinal centers, and number of germinal centers. Mass spectrometry comparing mouse B220+ splenocytes in Mb1CRE/WT; Ubr5fl/fl compared to Mb1CRE/WT; Ubr5+/+ mice showed that UBR5 in B cells in Mb1CRE/WT; Ubr5fl/fl mice has over two-fold more expression. Additionally, IgD was the most downregulated protein, B cell specific proteins were downregulated, and proteins involved with mRNA splicing were upregulated within the mass spectrometry. The loss of the UBR5 HECT domain leads to increased UBR5 half-life and upregulation of spliceosome proteins. Coupled together, this suggests that the loss of the carboxy terminus of UBR5 impedes B cell maturation by disrupting IgD expression, potentially by interfering with mRNA splicing. Finally, we have crossed and are currently aging our Mb1CRE/WT; Ubr5fl/fl mice with an EµCCND1 mouse model to determine if Ubr5 mutations lead to tumorigenesis. These studies aim to identify the role of UBR5 in the context of normal B cell development and lymphomagenesis with the goal of identifying therapeutic targets for drug discovery. Disclosures No relevant conflicts of interest to declare.

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Hasipek, Metis, Dale Grabowski, Yihong Guan, Anand D. Tiwari, Xiaorong Gu, Jason Valent, Jaroslaw Maciejewski, Frederic Joel Reu, James G. Phillips, and Babal K. Jha. "A Novel Therapeutic Strategy for Preferential Elimination of Multiple Myeloma Cells By Targeting Protein Disulfide Isomerase." Blood 136, Supplement 1 (November 5, 2020): 32–33. http://dx.doi.org/10.1182/blood-2020-142847.

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Multiple myeloma (MM) is a genetically complex hematological disease which is characterized by clonal proliferation of plasma cells in the bone marrow and secretion of monoclonal antibodies and cytokines that can damage bone, bone marrow, and kidney function1. MM cells constantly operate at the limit of their unfolded protein response (UPR) in the face of a secretory load of immunoglobin (Ig) and cytokines that is unparalleled by any other mammalian cell 2,3 and microenvironmental factors that aggravate the degree of physiologic misfolding that occurs during synthesis of secreted proteins. The endoplasmic reticulum (ER) resident protein disulfide isomerases (PDIs) are indispensable for folding of secreted proteins that require intramolecular disulfide-bond arrangement 4 like antibodies and many cytokines. As the main PDI family member, near-complete function of PDIA1 is essential for survival of MM cells while its inhibition should be manageable by the UPR in normal cells creating an opportunity for a large therapeutic window for PDI inhibitors in MM. Previously, we discovered and characterized an irreversible PDI inhibitor (CCF642) that induced cell death in MM cells at doses that did not affect survival of normal bone marrow cells. However, CCF642 has poor solubility and suboptimal selectivity precluding clinical translation. Using structure guided medicinal chemistry, we developed and characterized a highly potent and selective PDI inhibitor, with 10-fold higher potency (Fig 1B) and selectivity. CCF642-34 showed remarkable selectivity against PDIA1 and off-target bindings were eliminated when compared to CCF642 (Fig 1C). In addition to improved selectivity and in vitro PDI inhibition, CCF642-34 demonstrated more than 3-fold higher potency compared to CCF642 against MM1.S and bortezomib resistant MM1.S cells remained sensitive to CCF642-34. Importantly, the novel analogue CCF642-34 has 18-fold better potency in restricting the colony forming abilities of RPMI1640 cells while at no effect on the clonogenic potential of CD34+ cells derived from healthy bone marrow was observed at equivalent doses. CCF642-34 induces ER stress in MM1.S cells as observed in dose and time dependent cleavage of XBP1, IRE1α oligomerization and the profound induction of programmed cell death reflected by PARP and caspase 3 cleavage. To further analyze the modes of action of CCF642-34 and CCF642 we performed RNAseq after treatment of MM1.S cells and found exclusive induction of genes associated with UPR and downstream cell cycle and apoptotic responses for CCF642-34 while additional genes affecting were detected after CCF642 treatment. There were 362 and 568 differentially expressed genes in CCF642-34 and CCF-642 (compared to controls) treated MM1.S cells, respectively. Among these differentially expressed genes 87 down regulated and 142 upregulated were common to both, including downregulation of cell division and mitotic cell cycle process, and upregulation of response to ER stress, unfolded protein response, and apoptotic process gene sets. Results confirm that both CCF642 and CCF642-34 treatment act by inducing lethal ER-stress with greater selectivity for CCF642-34. Accordingly, hierarchical clustering showed distinct gene expression profiles in 642-34 and 642 treated MM1S cells (Fig. 2). CCF642-34 is orally bioavailable and highly efficacious in against established multiple myeloma in a syngeneic 5TGM1-luc/C57BL/KaLwRij model of myeloma. All vehicle control animals were dead by 52 days while 3 out of 6 mice lived beyond 6 months with no sign of relapse. In summary, we synthesized and characterized a novel lead PDIA1 inhibitor based on structure-guided medicinal chemistry that has improved pharmacologic properties to act as novel lead for clinical translation. References: 1. Manier S, Salem KZ, Park J, et al. Genomic complexity of multiple myeloma and its clinical implications. Nat. Rev. Clin. Oncol. 2017; 2. Fonseca R, Bergsagel PL, Drach J, et al. International Myeloma Working Group molecular classification of multiple myeloma: Spotlight review. Leukemia. 2009; 3. Wang M, Kaufman RJ. The impact of the endoplasmic reticulum protein-folding environment on cancer development. Nat. Rev. Cancer. 2014; 4. Freedman RB, Hirst TR, Tuite MF. Protein disulphide isomerase: building bridges in protein folding. Trends Biochem. Sci. 1994; Disclosures Valent: Takeda Pharmaceuticals: Other: Teaching, Speakers Bureau; Celgene: Other: Teaching, Speakers Bureau; Amgen Inc.: Other: Teaching, Speakers Bureau.

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Edwards, Donna R., Pei-yu Kuo, Alessandro Lagana, Seongjee Park, Pavithra Nedumaran, Violetta Leshchenko, Stephanie Christie, Shashidhar Jatiani, Julie Teruya-Feldstein, and Samir Parekh. "Aberrant Cell Cycle Programming Confers Rapid Lethality in the EuSOX11+ CCND1 MCL Mouse Model." Blood 136, Supplement 1 (November 5, 2020): 6–7. http://dx.doi.org/10.1182/blood-2020-143038.

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Mantle Cell Lymphoma (MCL) is characterized by the t(11;14)(q13;q32) translocation. This hallmark oncogenic event transposes CCND1 (11q13) under the control of the immunoglobin heavy chain (IGH) locus (14q32) resulting in constitutive cyclin D1 expression. Although Cyclin D1 (CCND1) overexpression is a key hallmark of MCL, CCND1 overexpressing murine models do not effectively recapitulate the MCL phenotype. Our published data demonstrated that SOX11 binds and regulates components in multiple oncogenic pathways in MCL (Kuo et. al., Oncogene 2015). Furthermore, we recently demonstrated that SOX11 promotes BCR signaling to drive MCL-like pathogenesis utilizing a SOX11 overexpressing (Eu-SOX11) murine model (Kuo et. al., Blood 2018). Given that the majority of classic human MCL co-express CCND1 and SOX11, we hypothesize that these oncogenes may cooperate to drive the pathogenesis of classical MCL. To study in vivo cooperation between CCND1 and SOX11, we crossed Eu-SOX11 mice with Eu-CCND1 mice to generate Eu-SOX11:CCND1 double transgenic (DT) mice. We have previously reported an significant increase in the fraction of CD5+CD19+CD23- MCL cells in the peripheral blood, spleens, lymph nodes and bone marrow of Eu-SOX11 mice and this fraction was further enhanced in DT mice (Fig.1A). We have now conducted a 2-year survival analysis on all 4 genotypes and found significantly reduced survival in DT as compared to Eu-SOX11 mice (Fig.1B). Median survival in DT mice is 16.5 months as compared to 19.7 months in Eu-SOX11 mice. Taken together, our results demonstrate a B-cell specific in vivo cooperation between SOX11 and CCND1 towards promoting a lethal MCL phenotype. RNA sequencing of splenocytes from DT versus SOX11-Tg mice showed significant enrichment of E2F1 target genes (p<.02) as a top oncogenic pathway (Fig.1C). Our previous results with CDK4/6 inhibition demonstrate a profound reduction in S phase in MCL cells (Divakar et. al., Leukemia 2016). We have developed small molecule SOX11 inhibitors using a SOX11-DNA homology model we built using the crystal structure of the SOX4-DNA binding domain as a template. SOX11 small molecular inhibitors in combination with CDK4 inhibitors will be used to further dissect the mechanism of cooperation between SOX11 and CCND1 and develop a therapeutic strategy for MCL that is mechanistically distinct from BTK or Bcl-2 inhibition. Disclosures Teruya-Feldstein: Edge Anthem: Consultancy. Parekh:Karyopharm: Research Funding; Celgene: Research Funding; Foundation Medicine: Consultancy.

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Bu, Yongqian, Caiwen Jia, Xiaowei Tian, Kalibixiati Aimulajiang, Muhammad Ali Memon, Ruofeng Yan, Xiaokai Song, Lixin Xu, and Xiangrui Li. "Immunization of Goats with Recombinant Protein 14-3-3 Isoform 2(rHcftt-2) Induced Moderate Protection against Haemonchus contortus Challenge." Pathogens 9, no. 1 (January 6, 2020): 46. http://dx.doi.org/10.3390/pathogens9010046.

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A previous study identified that isoform 2 (Hcftt-2) of the 14-3-3 protein of Haemonchus contortus (H. contortus) could suppress immune functions of goat peripheral blood mononuclear cells (PBMCs) and might be a potential vaccine target, as neutralization of the protein function may enhance anti-parasite immunity. In this research, the recombinant Hcftt-2 was evaluated for its immunoprotective efficacy against H. contortus infection in goats. Five experimental goats were immunized twice with rHcftt-2 along with Freund’s adjuvant. The five immunized goats and five nonimmunized goats (adjuvant only) were challenged with 5000 L3-stage H. contortus larvae after 14 days of second immunization. Five nonimmunized and uninfected goats (adjuvant only) were set as the uninfected group. A significant increase in the serum immunoglobin G(IgG) and serum IgA levels were identified in the rHcftt-2 immunized animals. The mean eggs per gram in feces (EPG) and the worm burdens of rHcftt-2 immunized group were reduced by 26.46% (p < 0.05) and 32.33%, respectively. In brief, immunization of goats with rHcftt-2 induced moderate protection against H. contortus challenge.

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Wake, Matthew, Jonathan Papworth, Luke Bayliss, Benjamin Grimshaw, Natalie Rynkiewicz, Jemima Paterson, Alicia Poindron, et al. "Generation and Characterisation of KY1066, a Fully Human Antibody Targeting the Enzymatic Activity of Matriptase-2 for the Treatment of Iron Overload in Beta Thalassemia." Blood 134, Supplement_1 (November 13, 2019): 3532. http://dx.doi.org/10.1182/blood-2019-124075.

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Beta thalassemia is an inherited hemoglobinopathy caused by a genetic defect in beta-globin gene and characterised by ineffective erythropoiesis, iron overload, splenomegaly and anemia. Excessive EPO production, resulting from the anemia, has a suppressive effect on the iron regulator hepcidin leading to increased iron absorption from the gut and release from internal stores. This in turn leads to tissue iron overload in transfusion independent (NTDT) patients and exacerbates the situation in transfusion dependent (TDT) patients. Primary standard of care treatment for TDT patients involves regular blood transfusions resulting in secondary iron overload and toxic tissue damage caused by non-transferrin bound iron (NTBI), which requires iron chelator treatment. Although transfusions and iron chelation have improved TDT patient prognosis, the iron overload experienced by some patients today still represents an unmet clinical need. The role of TMPRSS6 in iron regulation is already well established and reducing Tmprss6 expression was shown to increase hepcidin expression, correcting the iron overload, splenomegaly and anemia in Hbbth3/+ mice (Guo et al, JCI, 2013). Here we describe a first-in-class antibody targeting MTP-2, termed KY1066, for the treatment of diseases of iron overload, such as beta thalassemia. Through immunising mice transgenic for human immunoglobin heavy and light chain variable regions with purified human MTP-2 extra-cellular domain (ECD) and full-length human MTP-2 expressed on cells, we were able to obtain cross-reactive, MTP-2-specific monoclonal antibodies (mAbs). Our lead molecule, KY1066, was found to be a cross-reactive neutraliser of MTP-2 enzymatic activity both in vitro and in vivo and mechanistically blocks MTP-2 through binding to the serine protease (SP) domain active site, preventing cleavage of substrates. As a result, it was seen to increase BMP/SMAD signalling and elevate levels of hepcidin expression from hepatocyte cells following a single I.P. dose (10 mg/kg) in C57BL/6J mice. The elevation of hepcidin decreased serum iron and transferrin saturation through increased internalisation and degradation of ferroportin. In Hbbth3/+ mice, a single I.P. dose (10 mg/kg) showed a decrease of 52% and 47% in serum iron and transferrin saturation (TSAT) respectively, at the 2-week timepoint. Furthermore, with repeat dosing, we were able to show consistent iron restriction in a Hbbth3/+ mice over multiple weeks. Together this provides evidence KY1066 has the potential to treat iron overloaded patients, such as in beta thalassemia, to improve the anemia and reduce the transfusion and iron chelation need. Disclosures Wake: Kymab Ltd: Employment, Equity Ownership. Papworth:Kymab Ltd: Employment, Equity Ownership. Bayliss:Kymab Ltd: Employment, Equity Ownership. Grimshaw:Kymab Ltd: Employment, Equity Ownership. Rynkiewicz:Kymab Ltd: Employment, Equity Ownership. Paterson:Kymab Ltd: Employment, Equity Ownership. Poindron:Kymab Ltd: Employment, Equity Ownership. Carter:Kymab Ltd: Employment. Hudson:Kymab Ltd: Employment, Equity Ownership. Theurl:Kymab Ltd: Consultancy, Equity Ownership. Germaschewski:Kymab Ltd.: Employment, Equity Ownership. Meynard:Kymab Ltd: Research Funding.

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Dissertations / Theses on the topic "Immunoglobin; Blood cells"

Freeman, Sylvie. "Studies on CD33 and sialoadhesin : sialic acid binding receptors of the haemopoietic system." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318544.

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Kim, Jong-won. "Signalling initiation by blood dendritic cell antigen 2, a novel immunoglobulin receptor on plasmacytoid dendritic cells." Thesis, Imperial College London, 2018. http://hdl.handle.net/10044/1/63862.

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The focus of this project is a human-specific C-type lectin with potential roles in cell signalling: blood dendritic cell antigen 2 (BDCA-2). BDCA-2, a plasmacytoid dendritic cell-specific molecular marker, has been evaluated as a therapeutic target against auto-immune disorders, because antibodies to BDCA-2 inhibit the production of type I interferon. Accordingly, key goals of the project were to identify endogenous ligands for BDCA-2, to characterise the mechanism of ligand binding and ultimately to determine how ligands stimulate signalling pathways. A combination of BDCA-2 affinity chromatography column and mass spectrometry revealed that α2 macroglobulin and immunoglobulins, IgA, IgM and IgG are potential endogenous ligands in human serum. Competition binding studies conducted to characterise the binding affinity for each glycoprotein demonstrated that IgA has the highest affinity. Strategies for biochemical development of defined glycoforms of IgG Fc domain were established. The Chinese hamster ovary cell system for expression of Fc domain and the activity of enzymes necessary for chemoenzymatic glycoengineering have been tested. BDCA2 organisation in the cell membrane was studied by development of a transfected cell system which was analysed by affinity purification of BDCA-2 followed by analysis of protein-protein interactions. The results demonstrate that it is likely that BDCA-2 assembles with Fc receptor γ-chain in a 2:2 complex.

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Pain, Elisabeth. "Investigation of the immunomodulatory properties of intravenous immunoglobulin G (IVIg)." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251131.

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Petrez, J. H. "The transcytosis of polymeric immunoglobulin A and its receptor across the liver cell." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.330027.

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Sihra, Bhupinder Singh. "Studies investigating peripheral blood derived cells that express the high affinity receptor for immunoglobulin E (FceRI) in allergic disorders." Thesis, University of Southampton, 2008. https://eprints.soton.ac.uk/67619/.

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It is just forty years since the identification of immunoglobulin E (IgE) as the reagin responsible for allergen induced immediate hypersensitivity reactions. IgE exerts its biological actions through the binding of its Fc fragment to specific Fc receptors on effector cells. There are two predominant Fc receptors for IgE – FcεRI, which has a very high affinity for IgE and FcεRII, which shows less avid binding. For much of the first two decades after the identification of IgE, it was thought that FcεRI expression was limited to mast cells and basophils and that IgE binding to other cell types such as Blymphocytes and antigen presenting cells (APCs) was mainly due to FcεRII. However with major advances in characterisation and functional knowledge of FcεRI, particularly in the last fifteen years, it has become apparent that FcεRI can be expressed on several more cell types that may be involved in initiation and maintenance of allergic inflammation – including APCs (monocytes and dendritic cells) and possibly eosinophils. The research described in the four papers forming this thesis was completed during this period and evaluated FcεRI expression on different cell types, their potential roles in allergen induced inflammatory responses and whether successful therapeutic strategies for allergic disorders may involve actions on FcεRI+ cells. The relative expression of FcεRI on peripheral blood basophils, monocytes and eosinophils from atopic and non-atopic subjects and any relationship with serum IgE concentrations was assessed in the first paper. The second study examined a potentially important role for basophils as a cellular source of rapidly releasable IL-4 which may help initiate allergen induced TH2 responses. The next study investigated the possible effects on allergen induced early and late asthmatic responses of the immunosuppressive drug cyclosporin A which had been shown both to inhibit mast cell and basophil degranulation and cytokine secretion (particularly by CD4+ T-cells). The final study evaluated FcεRI expression on these cell types as well humoral factors (e.g. seasonal changes in allergen specific IgG and IgE) in subjects who, after 3 to 4 years of grass pollen immunotherapy, had continued on either active or placebo immunotherapy for a further 3 years. A historical perspective explaining some of the reasons the studies were done is provided in the introductory chapter whilst the discussion chapter at the end reviews how many of the findings of the study have evolved in subsequent years right up to the present day and finishes off with a brief synopsis of how rapidly increasing knowledge of the regulatory functions of dendritic cells (expressing FcεRI and often monocyte derived) has resulted in better understanding of the mechanisms of allergen specific immunotherapy and is leading to more effective treatment modalities.

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Pan, Han-En, and 潘漢恩. "Cytokine Profile in Peripheral Blood Mononuclear Cells of Immune-mediated Hemolytic Anemia Affected Dogs Intravenous Administration with Human Immunoglobulin." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/04157560056497689814.

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碩士
國立臺灣大學
獸醫學研究所
90
Immune-mediated hemolytic anemia (IMHA) is a common cause of severe anemia in dogs. The disease is characterized by accelerating destruction or removal of red blood cells (RBC) due to presence of anti-RBC autoantibodies with or without complement involvement. Conventional treatment with high dose corticosteroids and other cytotoxic drugs may be difficult or impossible to control IMHA, and the adverse effects may be severe. Intravenous administration of human immunoglobulin (IVIG), however, is efficacious in the treatment of human or canine IMHA. The immunopathogenic mechanisms underlying IMHA are still unknown, although evidence suggests that regulatory cytokines may play an important role. The respective contribution of the Th-1 and Th-2 cytokines is still a matter of debate. Even if several mechanisms of action have been proposed, a clear description of the relevant immunomodulatory effects by IVIG in canine IMHA is still scanty. This study was designed to investigate expression of cytokine mRNA from peripheral blood mononuclear cells (PBMC) before and after therapy with IVIG in dogs with IMHA. Blood samples from IMHA dogs were collected in pre and 1, 2, 4, 8, 16, 24 weeks post IVIG therapy. PBMC was collected from blood through Ficoll-Paque® separation and total RNA was extracted by TRIzol® purification. Cytokine gene expression was measured by reverse transcription and polymerase chain reaction (RT-PCR) and standardized by the amounts of internal housekeeping gene G3PDH expression in each sample. This semiquantitative assay was performed by densitometry on the electrophoresis picture of RT-PCR products. The cytokines IFN-γ, IL-2, IL-4, and IL-10 gene expression in naive and 2 μg/mL concanavalin A (Con A)-stimulated PBMC of IMHA dogs and control dogs were compared. Eight IMHA dogs, four idiopathic and four secondary IMHA, were included and all were administrated with 1 g/kg IVIG. The results showed IVIG therapy might be a beneficial alternative treatment for idiopathic IMHA dogs. Although we can’t demonstrate the Th-2-like dominant profile in IMHA dogs as in human or rodent disease, IL-2 gene expression in idiopathic IMHA dogs was statistically decreased. In addition, the ratio of IL-10/IL-2 in those dogs was significantly higher which suggests IMHA dog might have a relative dominance of Th-2 cytokine profile. The therapeutic effect of IVIG was complicated. The cytokine profile was mild increased in naive group but was partially diminishing in ConA-stimulated group. Eventually, most of the cytokines examined in IMHA affected dogs were gradually returned to the normal level 24 weeks after IVIG therapy. These results suggest that imbalance of cytokine network may relate to the pathogenesis of IMHA. Administration of IVIG may correct this irregulation and achieve its therapeutic effect.

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Bazzazan, Ali. "Levels of immunoglobulin G, white blood cells and fibrinogen in dairy cows with and without endometritis during the transitional period." Thèse, 2018. http://hdl.handle.net/1866/21071.

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Daniella, Perri. "The Role of Intravenous Immunoglobulin Anti-A and Anti-B in Complement Activation and Red Blood Cell Phagocytosis." Thesis, 2009. http://hdl.handle.net/1807/18976.

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Intravenous immunoglobulin is a human blood derived product that is used to treat immunodeficiencies and autoimmune disorders. An adverse side effect of IVIg therapy is hemolysis. Patients who experience hemolysis are mainly blood group A or AB. Clinical laboratory studies have demonstrated that IVIg contains ABO blood group antibodies, which can bind complement proteins. This study hypothesizes that anti-A/B in IVIg will bind to A/B antigens and activate complement in a dose dependant manner, which may lead to enhanced RBC phagocytosis. This study observed that the quantity of ABO antigens does not affect the in vitro binding of IVIg to RBCs. IVIg induced C3b deposition at high doses; however, the amount of complement deposition was insufficient to enhance phagocytosis of IVIg-sensitized RBCs by monocytic THP-1 cells in vitro. These studies emphasize that hemolytic reactions involve many factors in conjunction with antibodies and complement proteins.

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Chen, Se-man, and 陳瑟曼. "Effects of In-line skating around the island on white blood cell counts and the concentration of immunoglobulin." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/sgx7er.

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碩士
國立臺灣師範大學
體育學系
97
Many researchers concerned the change of immunity when we were undertaken different exercise or training in different forms, duration, load. We knew some biochemical researches about endurance exercises liked cycling and marathon, but there were few researches about in-line skating. Hence, the present studied was focused on clarifying the effects of In-line skating around the island on white blood cell counts and the concentration of immunoglobulin. 　Nine male subjects (age = 20.78 ± 2.22years, VO2max = 54.49 ± 5.87 ml•min-1•kg-1) engaged in 7-day In-line skating around the island (distance = 953 km). Blood sample were collected at the 1st, 4th, 7th day before exercise around the island, immediately exhaustive exercise at the 1st, 7th day, and 36 hours, 10 days after exercise. Compared with the variation in leukocyte count, neutrophil count, lymphocyte count, monocyte count, and in the concentration of immunoglobulin A (IgA), immunoglobulin G (IgG), immunoglobulin M (IgM). The rates of upper respiratory tract infections (URTI) were recorded. Data were analyzed using repeated one-way ANOVA and Pair-Sample t test. Result: 1) Lymphocyte count, concentration of IgA, IgG, IgM at the 4th, 7th day were significant lower than the 1st day (p< .05) in the exercise of 7-day In-line skating around the island. 2) After the day around the island, leukocyte count, neutrophil count and monocyte count were higher than before significantly (p< .05), but lymphocyte count was lower significantly at the 7th day. 3) The rate of URTI increased in the exercise of 7-day In-line skating around the island and the next week after exercise, but the change were no significant. (p> .05) With the days around the island went by, the immune cell showed a tendency to fall and the immunity reduced after the long time and endurance exercise. Thus the ratio of infection may increase.

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Books on the topic "Immunoglobin; Blood cells"

Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Blood transfusion. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0017.

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Introduction - Using the blood transfusion laboratory - Transfusion of red blood cells - Platelet transfusion - Fresh frozen plasma - Intravenous immunoglobulin - Transfusion transmitted infections - Irradiated blood products - Strategies for reducing blood transfusion in surgery - Maximum surgical blood ordering schedule (MSBOS) - Patients refusing blood transfusion for religious reasons, i.e. Jehovah’s Witnesses

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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, Shubha Allard, and Mammit Kaur. Blood transfusion. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0017_update_001.

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Ronco, Pierre M. Kidney involvement in plasma cell dyscrasias. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0150.

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Monoclonal proliferations of the B-cell lineage are characterized by abnormal and uncontrolled expansion of a single clone of B cells at different maturation stages, with a variable degree of differentiation to immunoglobulin-secreting plasma cells. Therefore, they are usually associated with the production and secretion in blood of a monoclonal immunoglobulin and/or a fragment thereof which may become deposited in tissues. These deposits can take the form of casts (in myeloma cast nephropathy), crystals (in myeloma-associated Fanconi syndrome), fibrils (in light-chain and exceptional heavy-chain amyloidosis), or granular precipitates (in monoclonal immunoglobulin deposition disease). They may disrupt organ structure and function, inducing life-threatening complications. All of the pathologic entities related to immunoglobulin deposition principally involve the kidney, which is not only explained by the high levels of renal plasma flow and glomerular filtration rate, but also by the sieving properties of the glomerular capillary wall and by the prominent role of the renal tubule in LC handling and catabolism.The different renal (and other) manifestations are related to the unique physicochemical characteristics of each paraprotein or immunoglobulin fragment, and the rate of their production.

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Barsoum, Rashad S. Schistosomiasis. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0181_update_001.

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AbstractSchistosomes are blood flukes that parasitize humans, apes, cattle, and other animals. In these definitive hosts they are bisexual, and lay eggs which are shed to fresh water where they complete an asexual cycle in different snails, ending in the release of cercariae which infect the definitive hosts to complete the life cycle.Seven of over 100 species of schistosomes are human pathogens, causing disease in different organs depending on the parasite species. Racial and genetic factors are involved in susceptibility, severity, and sequelae of infection.Morbidity is induced by the host’s immune response to schistosomal antigens. The latter include tegument, microsomal, gut, and oval antigens. The former are important in the process of invasion and establishment of infection, oval antigens in formation of granulomata which lead to fibrosis in different sites, and the gut antigens constitute the main circulating antigens in established infection, leading to immune-complex disease, particularly in the kidneys. The host immunological response includes innate and adaptive mechanisms, the former being the front line responsible for removing 90% of the infecting cercarial load. Adaptive immunity includes a Th1 phase, dominated by activation of an acute inflammatory response, followed by a prolonged Th2 phase which is responsible for immunity to re-infection as well as progression of tissue injury. Switching from Th1 to Th2 phases is controlled by functional and morphological change in the antigen-presenting cells, which is achieved by molecules of host as well as parasitic origin.Many cells participate in parasite killing, but also in the induction of tissue injury. The most potent of these is the eosinophil, which by binding antibodies to the parasite, particularly immunoglobulin E, facilitates parasite elimination. However, this process is complex, including agonist as well as antagonist pathways, which provide escape mechanisms for the parasite to survive, thereby achieving a delicate balance that permits schistosomes to live for decades in the infected host.

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Book chapters on the topic "Immunoglobin; Blood cells"

Beishuizen, A., M.-A. J. Verhoeven, K. Hählen, E. R. van Wering, and J. J. M. van Dongen. "Differences in Immunoglobulin and T-Cell Receptor Gene Rearrangement Patterns in Acute Lymphoblastic Leukemia Between Diagnosis and Relapse." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 51–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78350-0_9.

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Mizutani, S., T. M. Ford, L. M. Wiedemann, L. C. Chan, A. J. W. Furley, M. F. Greaves, and H. V. Molgaard. "Involvement of the D Segment (DQ 52) Nearest to the J H Region in Immunoglobulin Gene Rearrangements of Lymphoid-Cell Precursors." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 320–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72624-8_67.

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Davies, FE, and KC Anderson. "Abnormalities in immunoglobulin synthesizing cells." In Blood and Bone Marrow Pathology, 451–69. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-7020-3147-2.00030-4.

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Zent, Clive S., and Aaron Polliack. "Chronic lymphocytic leukaemia." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay, 5302–10. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0526.

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Chronic lymphocytic leukaemia (CLL)/small lymphocytic lymphoma is the most prevalent lymphoid neoplasm in Europe and North America. The ‘cell of origin’ is a mature B lymphocyte with a rearranged immunoglobulin gene. CLL cells express modest amounts of surface immunoglobulin, and are characterized by defective apoptosis. The cause of CLL is unknown. Most patients show no specific clinical features of disease and are diagnosed during evaluation of an incidental finding of peripheral blood lymphocytosis, lymphadenopathy, or splenomegaly. A small percentage of patients (<10%) present with symptomatic disease resulting from (1) tissue accumulation of lymphocytes such as disfiguring lymphadenopathy, splenomegaly with abdominal discomfort, profound fatigue, drenching night sweats, weight loss, and fever; or (2) manifestations of marrow failure with cytopenias including anaemia and thrombocytopenia. All CLL patients have an increased risk of infection, autoimmune cytopenias, and second haematological (e.g. diffuse large B-cell lymphoma) and nonhaematological malignancies. Diagnosis is usually made by analysis of the immunophenotype of the monoclonal circulating cells in the peripheral blood. In patients with the small lymphocytic variant of CLL without a detectable circulating monoclonal B-cell population, the diagnosis is made using tissue from the bone marrow, lymph nodes, or spleen. Treatment—there is no standard curative therapy and patients should not be treated until they have progressive and symptomatic disease or develop anaemia or thrombocytopenia due to bone marrow failure. If a decision is made to treat, then the best initial treatment should be given, based on evaluation of the patient’s disease characteristics with specific attention to the integrity of TP53 (coding for p53) and patient fitness.

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Turner-Stokes, Tabitha, and Mark A. Little. "Membranoproliferative glomerulonephritis." In Oxford Textbook of Medicine, edited by John D. Firth, 4937–43. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0487.

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The key histological features of membranoproliferative glomerulonephritis (MPGN) are mesangial hypercellularity, endocapillary proliferation, and capillary wall remodelling. There are two main types: (1) immune complex-mediated disease—caused by chronic infection causing persistent antigenaemia (notably hepatitis C), autoimmune disease, or monoclonal immunoglobulin production by plasma cell dyscrasia, and a few ‘idiopathic’ cases; and (2) complement-mediated disease—caused by dysregulation of the alternative pathway of complement, including by C3 nephritic factor (C3Nef), an autoantibody that stabilizes the alternative pathway C3 convertase. Clinical presentation is varied, including nephrotic syndrome, episodic visible haematuria, hypertension/rapidly progressive glomerulonephritis, asymptomatic nonvisible haematuria, and chronic kidney disease. Treatment depends on the underlying disease. All patients should receive appropriate conservative measures (blood pressure control, angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker). Underlying infection or monoclonal gammopathy should be treated, when possible, in those with immune complex-mediated MPGN. Eculizumab may have a role in treatment of some patients with complement-mediated MPGN. Steroids and cyclophosphamide or mycophenolate mofetil are used in patients with severe idiopathic MPGN.

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K. Poddar, Mrinal, and Soumyabrata Banerjee. "Molecular Aspects of Pathophysiology of Platelet Receptors." In Platelets. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.92856.

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Receptor is a dynamic instrumental surface protein that helps to interact with specific molecules to respond accordingly. Platelet is the smallest in size among the blood components, but it plays many pivotal roles to maintain hemostasis involving its surface receptors. It (platelet) has cell adhesion receptors (e.g., integrins and glycoproteins), leucine-rich repeats receptors (e.g., TLRs, glycoprotein complex, and MMPs), selectins (e.g., CLEC, P-selectin, and CD), tetraspanins (e.g., CD and LAMP), transmembrane receptors (e.g., purinergic—P2Y and P2X1), prostaglandin receptors (e.g., TxA2, PGH2, and PGI2), immunoglobulin superfamily receptors (e.g., FcRγ and FcεR), etc. on its surface. The platelet receptors (e.g., glycoproteins, protease-activated receptors, and GPCRs) during platelet activation are over expressed and their granule contents are secreted (including neurotransmitters, cytokines, and chemokines) into circulation, which are found to be correlated with different physiological conditions. Interestingly, platelets promote metastasis through circulation protecting from cytolysis and endogenous immune surveillance involving several platelets receptors. The updated knowledge about different types of platelet receptors in all probable aspects, including their inter- and intra-signaling mechanisms, are discussed with respect to not only its (platelets) receptor type but also under different pathophysiological conditions.

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Clark, M. R. "[52] The detection and characterization of antigen-specific monoclonal antibodies using anti-immunoglobulin isotype antibodies coupled to red blood cells." In Immunochemical Techniques Part I: Hybridoma Technology and Monoclonal Antibodies, 548–56. Elsevier, 1986. http://dx.doi.org/10.1016/0076-6879(86)21054-x.

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"The effect of homologous blood transfusion on delayed hypersensitivity skin test response has been studied using tetanus and diphtheria toxoids, streptococcus, tuberculin, Proteus, Candida and trichophyton antigens (4). Postoperative skin test response area decreased 57% in transfused patients compared to a 38% decrease in untransfused patients. Since transfused and untransfused patients differed significantly in duration of surgery, preoperative blood hemoglobin and serum albumin, the authors reanalyzed their data with 64 pairs of patients matched for these variables with the same results. The predictive value of delayed hypersensitivity skin testing for sepsis and mortality has not been accepted by all investigators. Brown et al. (5) agree that anergic patients have significantly higher rates of sepsis and mortality than normal responders, however "careful study of the temporal relationship between skin reactions and clinical events in individual patients suggested that these differences were not of value in clinical practice. Abnormal reactions usually followed obvious complications such as sepsis or secondary hemorrhage rather than predicted them. Anergy to skin testing may be related to a circulating serum factor which appears after trauma and causes lymphocyte suppression. There is no proven association of blood transfusion with serum suppressive activity or with anergy. Infectious complications and hospital stay are both significantly related to immunosuppressive serum and anergy. Lymphocyte Subsets Lymphocytes, B cells, T cells, helper cells and suppresser cells drop significantly five days after surgery and the decline is twice as great in the transfused patients compared to the untransfused (6). Helper cell number declines in transfused patients cause the helper/suppresser ratio to decrease significantly despite a significant decline in suppresser cell number. Changes in cell numbers recover somewhat by ten days so the differences between transfused and untransfused patients are no longer statistically significant although cell numbers in transfused patients are still lower than those in untransfused patients. Lymphocyte responses to ConA and PHA decline significantly in transfused groups, remaining below preoperative levels even one year following surgery. Response to ConA and PHA and MLR's in untransfused patients are significantly higher than in transfused patients at 90 days and 45 - 60 days respectively. Significant declines in immunoglobulin G, A and M cells are noted postoperatively in both transfused and untransfused patients. Other authors have not observed consistent changes in lymphocyte subsets in relation to transfusion. Changes in the numbers of lymphocytes in the various subsets in relation to surgery with and without blood transfusions studied in patients tested before and after surgery and in patients tested one week following transfusion alone, surgery alone or both reveal no evidence of suppression of immunity by surgery or blood transfusion (7). Generally surgery is followed by significant decreases in peripheral blood lymphocyte numbers affecting all lymphocyte subsets to some degree. Declines in helper cell numbers are associated with a significant decrease in the helper/suppresser ratio. It is not clear if transfused patients exhibit greater declines in lymphocytes due to the transfusion, due to the operative trauma, or due to pre-existing anemia which caused physicians to transfuse blood." In Transfusion Immunology and Medicine, 293. CRC Press, 1995. http://dx.doi.org/10.1201/9781482273441-22.

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Conference papers on the topic "Immunoglobin; Blood cells"

Grabowski, E. F., and K. McKenny. "CHARACTERIZATION OF DISORDERS OF PLATELET-VESSEL WALL INTERACTION IN AN AGGREGOMETER INCORPORATING BLOOD FLOW PAST AN ENDOTHELIAL CELL MONOLAYER." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644537.

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Epi-fluorescence videomicroscopy permits real-time imaging of platelet (plt) adhesion-aggregation to a defined microinjury site of an endothelial cell monolayer (ECM) exposed to flowing blood. The fluorescent label is the TAB murine monoclonal antibody (courtesy of Dr. R.P. McEver) directed against human pit cp HB, together with a fluorescein-conjugated goat F(ab')2 against murine immunoglobulin. The combination assures specificity for pit membranes, yet leaves pit function intact. Bovine aortic ECM, grown on rectangular cover glasses, comprise one wall of a flow chamber mounted on a vertical microscope stage. A 6-0 sterile suture, drawn across the ECM in a direction transverse to flow, creates microinjuries of width 70 ± 15 (mean ± SD). Pit deposition is virtually absent upon intact and confluent regions of the ECM. On microinjury sites and at a shear rate of 270 sec-1, however, computer-enhanced images show pit adherence, aggregation, and embolization. Pretreatment of the ECM with 1.0 mMFC lysine acetyl salicylate, further, leads to a three-fold increase in aggregate length. ECM products inhibitable by aspirin, therefore, modulate adhesion-aggregation in disease and normal states under physiologic flow conditions. The Table shows that nercent coverage of the injury area, and mean aggregate length readily discriminate normal, post-aspirin, and von Willebrand's (vWD's) bloods. Aggregate length is reduced in vWD's blood to a greater degree (p<0.01) than by oral aspirin, while the latter is associated with a paradoxic increase (p<0.01) in single plt adhesion.

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Koller, U., I. Pabinger, K. Lechner, and W. Knapp. "HEAT INACTIVATED HIGHLY PURIFIED FACTOR VIII CONCENTRATE IN THE TREATMENT OF HEMOPHILIACS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644057.

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51 severe hemophiliacs who had previously been treated with not virus-inactivated intermediate purity factor VIII concentrates were divided into two groups according to their immunological status. Group A (n=23) consisted of patients with CD4/CD8 (helper/suppressor) T cell ratio of 1.0, group B (n=28) of . patients with a ratio of 1.0. In patients of group A treatment was switched in May 1983 to highly purified heat inactivated factor VIII concentrate (BEHRINGWERKE GmbH, Marburg) whereas patients of group B continued to receive intermediate purity factor VIII concentrate. In both groups laboratory tests (clinical investigation, routine liver function tests, differential blood count, lymphocyte subpopulations and quantitative immunoglobulin analysis) were performed in May 1983 and repeated 6, 12 and 18 months thereafter. In group A a significant reduction (p 0.005) of CD8 positive cells from 10587/μl (median) to 540/μl (18 months) was observed; no significant changes of CD8 positive cells occurred in group B. CD4/CD8 ratio rose from 0.58 to 0.86 in group A (p = 0.005) and remained unchanged in group B (1.38 versus 1.23). Serum IgG decreased in both groups but was more pronounced in group A. Thus treatment with heat inactivated highly purified factor VIII improved the immunological status of hemophiliacs with an inverse ratio. Retrospective analysis of antibodies to HIV, however, showed that most of the patients of group A were antibody positive (n=21), but the 2 negative patients remained negative. In group B of the 10 HIV negative patients one became positive, all others did not change. Whether this improvement of immunological laboratory findings is of clinical relevance, remains to be established, particularly with respect to the high incidence of antibody positive patients within group A.

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Southworth, Thomas, Umme Kolsum, Andrew Higham, Sriram Sridhar, Tuyet-Hang Pham, Paul Newbold, and Dave Singh. "Analysis of Immunoglobulin A and M gene expression and plasma cells in bronchial tissue from COPD patients with high blood eosinophil counts." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa4924.

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Book chapters on the topic "Immunoglobin; Blood cells"

Conference papers on the topic "Immunoglobin; Blood cells"