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Inhibition of IgG1 and IgE production by stimulation of the B cell CTLA-4 receptor

TitoloInhibition of IgG1 and IgE production by stimulation of the B cell CTLA-4 receptor
Tipo di pubblicazioneArticolo su Rivista peer-reviewed
Anno di Pubblicazione2000
AutoriPioli, Claudio, Gatta L., Ubaldi V., and Doria G.
RivistaJournal of Immunology
Volume165
Paginazione5530-5536
ISSN00221767
Parole chiaveanimal cell, Animals, Antibodies, Antigens, article, B lymphocyte, B lymphocyte activation, B-Lymphocytes, CD, CD40, CD40 antigen, Cells, controlled study, Cultured, cytotoxic T lymphocyte antigen 4, Differentiation, Down-Regulation, enzyme linked immunosorbent assay, Flow cytometry, IgE, immediate type hypersensitivity, Immunoconjugates, Immunoglobulin Constant Regions, Immunoglobulin E, Immunoglobulin epsilon-Chains, immunoglobulin G, immunoglobulin G1, immunoglobulin M, immunoglobulin production, Inbred C57BL, interleukin 4, Interleukin-4, lipopolysaccharide, Lipopolysaccharides, Lymphocyte Count, Messenger, messenger RNA, Mice, Monoclonal, mouse, NF-kappa B, nonhuman, priority journal, Receptors, reverse transcription polymerase chain reaction, RNA, signal transduction, STAT6 Transcription Factor, Trans-Activators
Abstract

Although a large amount of information is available on the activity of CTLA-4 in T cells, the role of this receptor in B cells has not been previously characterized. Our results show that CD40 or LPS stimulation in the presence of IL-4 induces CTLA-4 expression in purified B cells; the maximum level is reached in both membrane and intracellular compartments after 48-72 h. Engagement of the B cell CTLA-4 by immobilized mAb inhibits IgG1 and IgE production and reduces the frequency of IgG1- and IgE-expressing B cells. Cε and Cγ1 germline mRNA expression as well as NF-κB and STAT6 activation, events required for isotype switching, are also inhibited by CTLA-4 engagement. Together these findings show the critical role of CTLA-4 in the control of IL-4-driven isotype switching and suggest new approaches for modulating immediate-type hypersensitivity responses.

Note

cited By 46

URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-0034669916&partnerID=40&md5=6a6df6dbc35f5f979d5396fba8d4fc5c
Citation KeyPioli20005530