IL‐10‐driven immunoglobulin production by B lymphocytes from IgA‐deficient individuals correlates to infection proneness
In search for a possible explanation of the phenotypic heterogeneity in IgA deficiency, we studied the function of B cells from IgA‐deficient (IgAd) individuals. Two groups of IgAd individuals, one frequently infected and one clinically apparently healthy, as well as normal controls, were studied. P...
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Published in | Clinical and experimental immunology Vol. 104; no. 3; pp. 432 - 438 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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Oxford BSL
Blackwell Science Ltd
01.06.1996
Blackwell Blackwell Science Inc |
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Online Access | Get full text |
ISSN | 0009-9104 1365-2249 |
DOI | 10.1046/j.1365-2249.1996.38746.x |
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Abstract | In search for a possible explanation of the phenotypic heterogeneity in IgA deficiency, we studied the function of B cells from IgA‐deficient (IgAd) individuals. Two groups of IgAd individuals, one frequently infected and one clinically apparently healthy, as well as normal controls, were studied. Peripheral blood mononuclear cells (PBMC) and B cells from IgAd individuals and controls were cultured with Staphylococcus aureus Cowan I strain and with anti‐CD40 MoAb presented on the CD32‐transfected fibroblast cell line in the presence of IL‐10. In this experimental system PBMC and B cells from the infection‐prone IgAd individuals produced only minute amounts of IgA. In contrast, PBMC and B cells from healthy IgAd subjects secreted significantly more IgA1 and IgA2 in comparison with infection‐prone IgAd patients (P < 0.05). These data suggest that the abnormalities of B cell differentiation in IgAd could be of heterogeneous origin. Thus, whereas in healthy IgAd subjects IgA production may be efficiently up‐regulated in vitro by addition of IL‐10 to CD40‐activated B cell culture, the corresponding B cell differentiation does not occur in infection‐prone IgAd patients. These observations provide a conceptual framework for phenotypic heterogeneity in IgAd subjects. |
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AbstractList | In search for a possible explanation of the phenotypic heterogeneity in IgA deficiency, we studied the function of B cells from IgA-deficient (IgAd) individuals. Two groups of IgAd individuals, one frequently infected and one clinically apparently healthy, as well as normal controls, were studied. Peripheral blood mononuclear cells (PBMC) and B cells from IgAd individuals and controls were cultured with Staphylococcus aureus Cowan I strain and with anti-CD40 MoAb presented on the CD32-transfected fibroblast cell line in the presence of IL-10. In this experimental system PBMC and B cells from the infection-prone IgAd individuals produced only minute amounts of IgA. In contrast, PBMC and B cells from healthy IgAd subjects secreted significantly more IgA1 and IgA2 in comparison with infection-prone IgAd patients (P < 0.05). These data suggest that the abnormalities of B cell differentiation in IgAd could be of heterogeneous origin. Thus, whereas in healthy IgAd subjects IgA production may be efficiently up-regulated in vitro by addition of IL-10 to CD40-activated B cell culture, the corresponding B cell differentiation does not occur in infection-prone IgAd patients. These observations provide a conceptual framework for phenotypic heterogeneity in IgAd subjects. In search for a possible explanation of the phenotypic heterogeneity in IgA deficiency, we studied the function of B cells from IgA-deficient (IgAd) individuals. Two groups of IgAd individuals, one frequently infected and one clinically apparently healthy, as well as normal controls, were studied. Peripheral blood mononuclear cells (PBMC) and B cells from IgAd individuals and controls were cultured with Staphylococcus aureus Cowan I strain and with anti-CD40 MoAb presented on the CD32-transfected fibroblast cell line in the presence of IL-10. In this experimental system PBMC and B cells from the infection-prone IgAd individuals produced only minute amounts of IgA. In contrast, PBMC and B cells from healthy IgAd subjects secreted significantly more IgA1 and IgA2 in comparison with infection-prone IgAd patients ( P < 0.05). These data suggest that the abnormalities of B cell differentiation in IgAd could be of heterogeneous origin. Thus, whereas in healthy IgAd subjects IgA production may be efficiently up-regulated in vitro by addition of IL-10 to CD40-activated B cell culture, the corresponding B cell differentiation does not occur in infection-prone IgAd patients. These observations provide a conceptual framework for phenotypic heterogeneity in IgAd subjects. In search for a possible explanation of the phenotypic heterogeneity in IgA deficiency, we studied the function of B cells from IgA-deficient (IgAd) individuals. Two groups of IgAd individuals, one frequently infected and one clinically apparently healthy, as well as normal controls, were studied. Peripheral blood mononuclear cells (PBMC) and B cells from IgAd individuals and controls were cultured with Staphylococcus aureus Cowan I strain and with anti-CD40 MoAb presented on the CD32-transfected fibroblast cell line in the presence of IL-10. In this experimental system PBMC and B cells from the infection-prone IgAd individuals produced only minute amounts of IgA. In contrast, PBMC and B cells from healthy IgAd subjects secreted significantly more IgA1 and IgA2 in comparison with infection-prone IgAd patients (P < 0.05). These data suggest that the abnormalities of B cell differentiation in IgAd could be of heterogeneous origin. Thus, whereas in healthy IgAd subjects IgA production may be efficiently up-regulated in vitro by addition of IL-10 to CD40-activated B cell culture, the corresponding B cell differentiation does not occur in infection-prone IgAd patients. These observations provide a conceptual framework for phenotypic heterogeneity in IgAd subjects.In search for a possible explanation of the phenotypic heterogeneity in IgA deficiency, we studied the function of B cells from IgA-deficient (IgAd) individuals. Two groups of IgAd individuals, one frequently infected and one clinically apparently healthy, as well as normal controls, were studied. Peripheral blood mononuclear cells (PBMC) and B cells from IgAd individuals and controls were cultured with Staphylococcus aureus Cowan I strain and with anti-CD40 MoAb presented on the CD32-transfected fibroblast cell line in the presence of IL-10. In this experimental system PBMC and B cells from the infection-prone IgAd individuals produced only minute amounts of IgA. In contrast, PBMC and B cells from healthy IgAd subjects secreted significantly more IgA1 and IgA2 in comparison with infection-prone IgAd patients (P < 0.05). These data suggest that the abnormalities of B cell differentiation in IgAd could be of heterogeneous origin. Thus, whereas in healthy IgAd subjects IgA production may be efficiently up-regulated in vitro by addition of IL-10 to CD40-activated B cell culture, the corresponding B cell differentiation does not occur in infection-prone IgAd patients. These observations provide a conceptual framework for phenotypic heterogeneity in IgAd subjects. |
Author | HANSON, L. Å. TARKOWSKI, A. BRIDON, J.‐M. FRIMAN, V. BANCHEREAU, J. BRIÈRE, F. |
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Keywords | Human Immunopathology IgA Immunoglobulins Cell function Cytokine Biosynthesis B-Lymphocyte Immune deficiency In vitro Biological activity Phenotype Interleukin 10 |
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Snippet | In search for a possible explanation of the phenotypic heterogeneity in IgA deficiency, we studied the function of B cells from IgA‐deficient (IgAd)... In search for a possible explanation of the phenotypic heterogeneity in IgA deficiency, we studied the function of B cells from IgA-deficient (IgAd)... |
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SubjectTerms | Adult analysis Antibodies Antibodies, Monoclonal - immunology Antibody Formation B lymphocytes B-Lymphocytes - immunology Biological and medical sciences biosynthesis CD40 CD40 Antigens CD40 Antigens - immunology Cells Cells, Cultured Coculture Techniques Culture Media Culture Media - analysis Cultured Dysgammaglobulinemia Dysgammaglobulinemia - immunology Enzyme-Linked Immunosorbent Assay Female Fibroblasts genetics Humans IgA Deficiency IgA Deficiency - immunology IL‐10 Immunodeficiencies Immunodeficiencies. Immunoglobulinopathies Immunoglobulin A Immunoglobulin A - analysis Immunoglobulin A - biosynthesis Immunoglobulin G Immunoglobulin G - analysis Immunoglobulin G - biosynthesis Immunoglobulin M Immunoglobulin M - analysis Immunoglobulin M - biosynthesis immunoglobulin production immunology Immunopathology Infectious Medicine Infektionsmedicin Interleukin-10 Interleukin-10 - genetics Interleukin-10 - immunology Leukocytes Leukocytes, Mononuclear - immunology Lymphocyte Activation Male Medical sciences Middle Aged Monoclonal Mononuclear Original Recombinant Proteins Recombinant Proteins - immunology Respiratory Tract Infections Respiratory Tract Infections - immunology Staphylococcal Infections Staphylococcal Infections - immunology Staphylococcus aureus Transfection Up-Regulation |
Title | IL‐10‐driven immunoglobulin production by B lymphocytes from IgA‐deficient individuals correlates to infection proneness |
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