Interleukin 10 induces B lymphocytes from IgA-deficient patients to secrete IgA

• Published in: The Journal of clinical investigation Vol. 94; no. 1; pp. 97 - 104
• Main Authors: Brière, F, Bridon, J M, Chevet, D, Souillet, G, Bienvenu, F, Guret, C, Martinez-Valdez, H, Banchereau, J
• Format: Journal Article
• Language: English
• Published: United States 01-07-1994
• Subjects: Adolescent; Adult; Antibodies, Monoclonal - immunology; Antigens, CD - physiology; Antigens, Differentiation, B-Lymphocyte - physiology; B-Lymphocytes - drug effects; B-Lymphocytes - immunology; CD40 Antigens; Cells, Cultured; Child; Child, Preschool; Female; Humans; IgA Deficiency - immunology; Immunoglobulin A, Secretory - metabolism; Immunophenotyping; Interleukin-10 - pharmacology; Male
• ISSN: 0021-9738
• DOI: 10.1172/JCI117354

We have previously shown that human B lymphocytes cultured in the CD40 system, composed of an anti-CD40 mAb presented by a CD32-transfected fibroblastic cell line, proliferate but do not secrete antibodies. However, the addition of particles of Staphylococcus aureus Cowan (SAC) induces B cell differentiation even in the absence of exogenous cytokines (CD40/SAC system). Additionally, B lymphocytes cultured in the CD40 system in the presence of human IL-10, produce IgM, IgG, and IgA, and Ig levels are further increased by SAC. Here, we have studied the capacity of peripheral blood lymphocytes from patients with IgA deficiency (IgA-D) to secrete Igs, particularly IgA after CD40 triggering. Peripheral blood mononuclear cells (PBMNC) from IgA-D patients cultured in the CD40/SAC system produced IgM and IgG, but not IgA. The addition of IL-10 to the cultures, enhanced the production of IgM and IgG and most strikingly induced the production of high amounts of IgA. The addition of IL-10 to PBMNC from IgA-D patients activated through CD40 alone resulted in the production of IgA. Thus, SAC and anti-CD40 mAb stimulate B cells to differentiate into cells secreting IgG and IgM whereas IL-10 plays a central role in inducing B cells from IgA-D patients to differentiate into IgA secreting cells.