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J Veitch - One of the best experts on this subject based on the ideXlab platform.
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Immunoglobulin Subclass distribution and binding characteristics of anti gq1b antibodies in miller fisher syndrome
Journal of Neuroimmunology, 1994Co-Authors: Hugh J Willison, J VeitchAbstract:Circulating IgG antibodies to carbohydrate determinants on GQ1b ganglioside are found in the acute phase sera of patients with Miller Fisher syndrome, a variant of Guillain-Barre syndrome. Here we report that the IgG Subclass distribution of the anti-GQ1b antibodies is mainly restricted to IgG1 and IgG3 antibodies, Subclasses typically associated with a T cell-dependent immune response to protein antigens. This is highly unusual in that IgG responses to carbohydrate determinants are typically of the IgG2 Subclass. Anti-GQ1b antibodies also have a limited ability to bind GQ1b in a membrane-like environment, particularly at body temperature. These data suggest that the antigen initiating the immune response in MFS is not likely GQ1b but an unidentified cross-reactive glycoprotein antigen(s). Similar results were obtained for anti-GM1 IgG antibodies in Guillain-Barre syndrome.
Hugh J Willison - One of the best experts on this subject based on the ideXlab platform.
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Immunoglobulin Subclass distribution and binding characteristics of anti gq1b antibodies in miller fisher syndrome
Journal of Neuroimmunology, 1994Co-Authors: Hugh J Willison, J VeitchAbstract:Circulating IgG antibodies to carbohydrate determinants on GQ1b ganglioside are found in the acute phase sera of patients with Miller Fisher syndrome, a variant of Guillain-Barre syndrome. Here we report that the IgG Subclass distribution of the anti-GQ1b antibodies is mainly restricted to IgG1 and IgG3 antibodies, Subclasses typically associated with a T cell-dependent immune response to protein antigens. This is highly unusual in that IgG responses to carbohydrate determinants are typically of the IgG2 Subclass. Anti-GQ1b antibodies also have a limited ability to bind GQ1b in a membrane-like environment, particularly at body temperature. These data suggest that the antigen initiating the immune response in MFS is not likely GQ1b but an unidentified cross-reactive glycoprotein antigen(s). Similar results were obtained for anti-GM1 IgG antibodies in Guillain-Barre syndrome.
Elena Blanco - One of the best experts on this subject based on the ideXlab platform.
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defects in memory b cell and plasma cell subsets expressing different Immunoglobulin Subclasses in patients with cvid and Immunoglobulin Subclass deficiencies
The Journal of Allergy and Clinical Immunology, 2019Co-Authors: Elena Blanco, Martin Perezandres, Sonia Arribamendez, Cristina Serrano, Ignacio Criado, Lucia Del Pinomolina, Susana L SilvaAbstract:Background Predominantly antibody deficiencies (PADs) are the most prevalent primary immunodeficiencies, but their B-cell defects and underlying genetic alterations remain largely unknown. Objective We investigated patients with PADs for the distribution of 41 blood B-cell and plasma cell (PC) subsets, including subsets defined by expression of distinct Immunoglobulin heavy chain Subclasses. Methods Blood samples from 139 patients with PADs, 61 patients with common variable immunodeficiency (CVID), 68 patients with selective IgA deficiency (IgAdef), 10 patients with IgG Subclass deficiency with IgA deficiency, and 223 age-matched control subjects were studied by using flow cytometry with EuroFlow Immunoglobulin isotype staining. Patients were classified according to their B-cell and PC immune profile, and the obtained patient clusters were correlated with clinical manifestations of PADs. Results Decreased counts of blood PCs, memory B cells (MBCs), or both expressing distinct IgA and IgG Subclasses were identified in all patients with PADs. In patients with IgAdef, B-cell defects were mainly restricted to surface membrane (sm)IgA+ PCs and MBCs, with 2 clear subgroups showing strongly decreased numbers of smIgA+ PCs with mild versus severe smIgA+ MBC defects and higher frequencies of nonrespiratory tract infections, autoimmunity, and affected family members. Patients with IgG Subclass deficiency with IgA deficiency and those with CVID showed defects in both smIgA+ and smIgG+ MBCs and PCs. Reduced numbers of switched PCs were systematically found in patients with CVID (absent in 98%), with 6 different defective MBC (and clinical) profiles: (1) profound decrease in MBC numbers; (2) defective CD27+ MBCs with almost normal IgG3+ MBCs; (3) absence of switched MBCs; and (4) presence of both unswitched and switched MBCs without and; (5) with IgG2+ MBCs; and (6) with IgA1+ MBCs. Conclusion Distinct PAD defective B-cell patterns were identified that are associated with unique clinical profiles.
Caroline O S Savage - One of the best experts on this subject based on the ideXlab platform.
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Immunoglobulin Subclass determines ability of Immunoglobulin ig g to capture and activate neutrophils presented as normal human igg or disease associated anti neutrophil cytoplasm antibody anca igg
Clinical and Experimental Immunology, 2011Co-Authors: Tanya Pankhurst, Gerard B Nash, Julie M Williams, R Colman, Abdullah Hussain, Caroline O S SavageAbstract:Immunoglobulin G (IgG) is a potent neutrophil stimulus, particularly when presented as anti-neutrophil cytoplasm antibody (ANCA) in ANCA-associated vasculitis. We assessed whether IgG Subclasses had differential effects on neutrophil activation and whether differences were dependent on specific Fc-receptor engagement. Using a physiologically relevant flow model, we compared adhesion of neutrophils to different Subclasses of normal IgG coated onto solid surfaces, with adhesion of neutrophils treated with different Subclasses of soluble ANCA IgG to P-selectin surfaces or endothelial cells (EC). Normal IgG captured flowing neutrophils efficiently in the order IgG3 > IgG1 > IgG2 > IgG4. Fc-receptor blockade reduced capture, IgG3 being more dependent on CD16 and IgG1/2 on CD32. Blockade of the integrin CD18 reduced neutrophil spreading, while inhibition of calcium-dependent signalling reduced both capture and spreading, suggesting that both were active processes. Neutrophils treated with ANCA IgG Subclasses 1, 3 and 4 showed stabilization of adhesion to P-selectin surfaces and EC. ANCA changed neutrophil behaviour from rolling to static adhesion and the potency of the Subclasses followed the same pattern as above: IgG3 > IgG1 > IgG4. Blockade of Fc receptors resulted in neutrophils continuing to roll, i.e. they were not ANCA-activated; differential utilization of Fc receptor by particular IgG Subclasses was not as apparent as during neutrophil capture by normal IgG. IgG3 is the most effective Subclass for inducing neutrophil adhesion and altered behaviour, irrespective of whether the IgG is surface bound or docks onto neutrophil surface antigens prior to engaging Fc receptors. Engagement of Fc receptors underpins these responses; the dominant Fc receptor depends on IgG Subclass.
Susana L Silva - One of the best experts on this subject based on the ideXlab platform.
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defects in memory b cell and plasma cell subsets expressing different Immunoglobulin Subclasses in patients with cvid and Immunoglobulin Subclass deficiencies
The Journal of Allergy and Clinical Immunology, 2019Co-Authors: Elena Blanco, Martin Perezandres, Sonia Arribamendez, Cristina Serrano, Ignacio Criado, Lucia Del Pinomolina, Susana L SilvaAbstract:Background Predominantly antibody deficiencies (PADs) are the most prevalent primary immunodeficiencies, but their B-cell defects and underlying genetic alterations remain largely unknown. Objective We investigated patients with PADs for the distribution of 41 blood B-cell and plasma cell (PC) subsets, including subsets defined by expression of distinct Immunoglobulin heavy chain Subclasses. Methods Blood samples from 139 patients with PADs, 61 patients with common variable immunodeficiency (CVID), 68 patients with selective IgA deficiency (IgAdef), 10 patients with IgG Subclass deficiency with IgA deficiency, and 223 age-matched control subjects were studied by using flow cytometry with EuroFlow Immunoglobulin isotype staining. Patients were classified according to their B-cell and PC immune profile, and the obtained patient clusters were correlated with clinical manifestations of PADs. Results Decreased counts of blood PCs, memory B cells (MBCs), or both expressing distinct IgA and IgG Subclasses were identified in all patients with PADs. In patients with IgAdef, B-cell defects were mainly restricted to surface membrane (sm)IgA+ PCs and MBCs, with 2 clear subgroups showing strongly decreased numbers of smIgA+ PCs with mild versus severe smIgA+ MBC defects and higher frequencies of nonrespiratory tract infections, autoimmunity, and affected family members. Patients with IgG Subclass deficiency with IgA deficiency and those with CVID showed defects in both smIgA+ and smIgG+ MBCs and PCs. Reduced numbers of switched PCs were systematically found in patients with CVID (absent in 98%), with 6 different defective MBC (and clinical) profiles: (1) profound decrease in MBC numbers; (2) defective CD27+ MBCs with almost normal IgG3+ MBCs; (3) absence of switched MBCs; and (4) presence of both unswitched and switched MBCs without and; (5) with IgG2+ MBCs; and (6) with IgA1+ MBCs. Conclusion Distinct PAD defective B-cell patterns were identified that are associated with unique clinical profiles.
