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IL-10-driven immunoglobulin production by B lymphocytes from IgA-deficient individuals correlates to infection proneness.

Artikel i vetenskaplig tidskrift
Författare Vanda Friman
Lars Åke Hanson
J M Bridon
Andrej Tarkowski
J Banchereau
F Brière
Publicerad i Clinical and experimental immunology
Volym 104
Nummer/häfte 3
Sidor 432-8
ISSN 0009-9104
Publiceringsår 1996
Publicerad vid Institutionen för laboratoriemedicin, Avdelningen för klinisk immunologi
Institutionen för invärtesmedicin, Avdelningen för infektionssjukdomar
Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning
Sidor 432-8
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adult, Antibodies, Monoclonal, immunology, Antibody Formation, B-Lymphocytes, immunology, CD40 Antigens, immunology, Cells, Cultured, Coculture Techniques, Culture Media, analysis, Dysgammaglobulinemia, immunology, Enzyme-Linked Immunosorbent Assay, Female, Fibroblasts, Humans, IgA Deficiency, immunology, Immunoglobulin A, analysis, biosynthesis, Immunoglobulin G, analysis, biosynthesis, Immunoglobulin M, analysis, biosynthesis, Interleukin-10, genetics, immunology, Leukocytes, Mononuclear, immunology, Lymphocyte Activation, Male, Middle Aged, Recombinant Proteins, immunology, Respiratory Tract Infections, immunology, Staphylococcal Infections, immunology, Staphylococcus aureus, Transfection, Up-Regulation
Ämneskategorier Infektionsmedicin

Sammanfattning

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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