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 inClinical and experimental immunology Vol. 104; no. 3; pp. 432 - 438
Main Authors FRIMAN, V., HANSON, L. Å., BRIDON, J.‐M., TARKOWSKI, A., BANCHEREAU, J., BRIÈRE, F.
Format Journal Article
LanguageEnglish
Published Oxford BSL Blackwell Science Ltd 01.06.1996
Blackwell
Blackwell Science Inc
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ISSN0009-9104
1365-2249
DOI10.1046/j.1365-2249.1996.38746.x

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Summary: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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ISSN:0009-9104
1365-2249
DOI:10.1046/j.1365-2249.1996.38746.x