Inhibitory Receptors CD85j, LAIR-1, and CD152 Down-Regulate Immunoglobulin and Cytokine Production by Human B Lymphocytes
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Published:2005-06
Issue:6
Volume:12
Page:705-712
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ISSN:1556-6811
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Container-title:Clinical and Vaccine Immunology
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language:en
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Short-container-title:Clin Vaccine Immunol
Author:
Merlo Andrea1, Tenca Claudya1, Fais Franco1, Battini Lorenzo1, Ciccone Ermanno1, Grossi Carlo E.1, Saverino Daniele1
Affiliation:
1. Department of Experimental Medicine, Section of Human Anatomy, University of Genova, Via De Toni 14, 16132 Genova, Italy
Abstract
ABSTRACT
Class switching consists in the substitution of the heavy-chain constant region of immunoglobulin M (IgM) with that of IgG, IgA, or IgE. This enables antibodies to acquire new effector functions that are crucial to combat invading pathogens. Class switching usually requires engagement of CD40 on B cells by CD40 ligand (CD40L) on antigen-activated CD4
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T cells and the production of cytokines. The process must be regulated tightly because abnormal IgG and IgA production favors the onset of autoimmunity, whereas increased switching to IgE leads to atopy. These inflammatory disorders can be triggered or exacerbated by costimulatory signals. Although thoroughly investigated on T cells, the roles of the inhibitory receptors CD85j, LAIR-1, and CD152 on B-cell functions have not been fully elucidated. In this study we show that cross-linking of the B-cell inhibitory receptors by specific monoclonal antibodies inhibits IgG and IgE production, reduces the percentage of IgG- and IgE-expressing B cells, and down-regulates interleukin 8 (IL-8), IL-10, and tumor necrosis factor alpha production. These effects were demonstrated using different B-cell stimulatory pathways (recall antigens, CD40L-transfected cells plus IL-4, and lipopolysaccharide plus IL-4). It thus appears that CD85j, LAIR-1, and CD152 play a central role for the control of IL-4-driven isotype switching.
Publisher
American Society for Microbiology
Subject
Microbiology (medical),Clinical Biochemistry,Immunology,Immunology and Allergy
Reference34 articles.
1. Alter, A., M. Duddy, S. Hebert, K. Biernacki, A. Prat, J. P. Antel, V. W. Yong, R. K. Nuttall, C. J. Pennington, D. R. Edwards, and A. Bar-Or. 2003. Determinants of human B cell migration across brain endothelial cells. J. Immunol.170:4497-4505. 2. Binstadt, B. A., K. M. Brumbaugh, C. J. Dick, A. M. Scharenberg, B. L. Williams, M. Colonna, L. L. Lanier, J. P. Kinet, R. T. Abraham, and P. J. Leibson. 1996. Sequential involvement of Lck and SHP-1 with MHC-recognizing receptors on NK cells inhibits FcR-initiated tyrosine kinase activation. Immunity6:629-638. 3. Borges, L., M. L. Hsu, N. Fanger, M. Kubin, and D. Cosman. 1997. A family of human lymphoid and myeloid Ig-like receptors, some of which bind to MHC class I molecules. J. Immunol.159:5192-5196. 4. Brunner, M. C., C. A. Chambers, F. K. Chan, J. Hanke, A. Winoto, and J. P. Allison. 1999. CTLA-4-mediated inhibition of early events of T cell proliferation. J. Immunol.162:5813-5820. 5. Caux, C., C. Massacrier, B. Vanbervliet, C. Barthelemy, Y. J. Liu, and J. Banchereau. 1994. Interleukin 10 inhibits T cell alloreaction induced by human dendritic cells. Int. Immunol.6:1177-1185.
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