A new mouse anti-mouse complement receptor type 2 and 1 (CR2/CR1) monoclonal antibody as a tool to study receptor involvement in chronic models of immune responses and disease. Issue 2 (February 2015)

• Record Type: Journal Article
• Authors: Kulik, Liudmila; Hewitt, Finnegan B.; Willis, Van C.; Rodriguez, Rosa; Tomlinson, Stephen; Michael Holers, V.
• Is Part Of: Molecular immunology. Volume 63:Issue 2(2015:Feb.)
• Page Start: 479
• Page End: 488
• Publication Date: 2015-02
• Subjects: Immunochemistry -- Periodicals; Molecular biology -- Periodicals; Immunochemistry -- Periodicals; Allergy and Immunology -- Periodicals; Molecular Biology -- Periodicals; Immunochimie -- Périodiques; Biologie moléculaire -- Périodiques; Immunochemistry; Molecular biology; Periodicals; Electronic journals; 571.96
• DOI: 10.1016/j.molimm.2014.10.005
• Languages: English
• ISSNs: 0161-5890

Abstract

<abstract abstract-type="author-highlights" id="abs0005"> <title id="sect0005">Highlights</title> <sec> <p id="spar0005"> <list id="lis0005"> <list-item id="lsti0005"> <label></label> <p id="par0005">We generated a new monoclonal mouse anti-mouse complement receptor type 2/complement receptor type 1 (CR2/CR1) antibody, designated mAb 4B2.</p> </list-item> <list-item id="lsti0010"> <label></label> <p id="par0010">mAb 4B2 antibody blocks binding of the C3dg ligand to CR2.</p> </list-item> <list-item id="lsti0015"> <label></label> <p id="par0015"> <italic>In vivo</italic> injected mAb 4B2 induces partial down regulation of CR1 and a more substantial elimination of CR2 from B cells without inducing B cell death or elimination.</p> </list-item> <list-item id="lsti0020"> <label></label> <p id="par0020"> <italic>In vivo</italic> injection of mAb 4B2 antibody decreases humoral immune responses to T dependent antigens.</p> </list-item> <list-item id="lsti0025"> <label></label> <p id="par0025">mAb 4B2 can be used at various time points in murine chronic models of human autoimmune and inflammatory diseases to assess the role of receptor-ligand interactions in the further evolution of disease.</p> </list-item> </list> </p> </sec> </abstract>