Regulation of immunoglobulin secretion by factor H of human complement.

TitleRegulation of immunoglobulin secretion by factor H of human complement.
Publication TypeJournal Article
Year of Publication1985
AuthorsTsokos GC, Inghirami G, Tsoukas CD, Balow JE, Lambris JD
Date Published1985 Jul
KeywordsAntibody-Producing Cells, B-Lymphocytes, Cell Transformation, Viral, Complement C3b Inactivator Proteins, Complement Factor H, Hemolytic Plaque Technique, Herpesvirus 4, Human, Humans, Immune Tolerance, Immunoglobulins, Lymphocyte Activation, Pokeweed Mitogens, T-Lymphocytes, Regulatory

As human B lymphocytes and macrophages carry surface receptors for Factor H (B1H), we investigated the possibility that this complement component regulates their function. Factor H inhibits immunoglobulin secretion by peripheral mononuclear cells (MNC) stimulated with pokeweed mitogen if present at the initiation of the cultures and at concentrations greater than 50 micrograms/ml. Factor H also inhibited stimulation and differentiation of purified B cells into immunoglobulin-secreting cells by Epstein-Barr virus (EBV). The inhibitory effect of Factor H was abrogated if anti-Factor H antibody was present in the cultures. EBV-transformed B-cell lines secreted less immunoglobulin if Factor H was present in the culture for at least 4 days. Culture of MNC with Factor H did not lead to the generation of suppressor T cells or macrophages. In contrast, Factor H did not cause proliferation of human peripheral total MNC or enriched T-cell or B-cell subpopulations. Also, Factor H did not inhibit the proliferation of MNC in response to several mitogens and antigens. Our results strongly indicate that Factor H is able to block human B-cell differentiation in vitro without blocking the proliferative ability of the cells. Factor H seems to act directly on the B cells through its receptor on their surface, since it inhibited T-dependent and T-independent B-cell differentiation but generated no suppressor cells.

Alternate JournalImmunology
PubMed ID2991125
PubMed Central IDPMC1453630
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