Complement receptors (CR) and cytotoxic responses: monoclonal antibodies directed against CR1 and CR3 inhibit the generation of human allospecific and virus specific cytotoxic cells in vitro.

TitleComplement receptors (CR) and cytotoxic responses: monoclonal antibodies directed against CR1 and CR3 inhibit the generation of human allospecific and virus specific cytotoxic cells in vitro.
Publication TypeJournal Article
Year of Publication1986
AuthorsInghirami G, Lambris JD, Tsokos GC
JournalJ Immunopharmacol
Volume8
Issue1
Pagination75-88
Date Published1986
ISSN0163-0571
KeywordsAntibodies, Monoclonal, Antibody Specificity, Cell Line, Cytotoxicity, Immunologic, Dose-Response Relationship, Drug, Herpesvirus 4, Human, Histocompatibility Antigens Class II, HLA-DR Antigens, Humans, Kinetics, Lymphocyte Culture Test, Mixed, Receptors, Complement, Receptors, Complement 3b, T-Lymphocytes, Cytotoxic, T-Lymphocytes, Helper-Inducer, Time Factors
Abstract

A variety of cellular immune responses involve complement factors which bind to specific receptors, and modulate or effect a specific reaction. Monoclonal antibodies (MAb) have been generated against complement receptors (CR) 1 and 3, which were utilized to investigate human allogeneic and Epstein-Barr virus specific cytotoxic cells in vitro. MAb OKM1, which binds to the C3bi CR (CR3), and MAb M710, which binds to the C3b/4b CR (CR1), inhibited the generation of both allogeneic and virus specific cytotoxic responses in vitro in a dose-dependent way; doses of 1 microgram/ml (or greater) completely abrogated the cytotoxic responses. Inhibition of these responses was observed when the MAb was added to the cultures at any time point except the last two days. In addition, treatment of the responder (but not the stimulator cells) with either MAb resulted in complete inhibition of cytotoxic responses. These experiment indicate that complement receptors participate in the generation of human cytotoxic responses in vitro.

DOI10.3109/08923978609031086
Alternate JournalJ Immunopharmacol
PubMed ID3011915
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