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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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.
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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Issue 3
Keywords Human
Immunopathology
IgA
Immunoglobulins
Cell function
Cytokine
Biosynthesis
B-Lymphocyte
Immune deficiency
In vitro
Biological activity
Phenotype
Interleukin 10
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PublicationTitle Clinical and experimental immunology
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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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