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Human monoclonal natural autoantibodies against the T‐cell receptor inhibit interleukin‐2 production in murine T cells
Author(s) -
Robey Ian F.,
Schluter Samuel F.,
Akporiaye Emmanuel,
Yocum David E.,
Marchalonis John J.
Publication year - 2002
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2002.01389.x
Subject(s) - t cell receptor , autoantibody , epitope , immunology , monoclonal antibody , biology , t cell , clone (java method) , isotype , monoclonal , antigen , microbiology and biotechnology , antibody , immune system , dna , genetics
Summary Natural autoantibodies (NAAbs) specific for the T‐cell receptor (TCR) are present in all human sera, but individuals with rheumatoid arthritis (RA) generally produce higher titres of immunoglobulin M (IgM) isotype autoantibodies (AAbs) against Vβ TCR epitopes. To investigate possible correlations between the specificity of such AAbs and their role in immunomodulation, we generated seven B‐cell hetero‐hybridomas, secreting monoclonal IgM NAAbs, from the synovial tissue and peripheral blood of patients with RA. Here we report three anti‐TCR monoclonal autoantibodies (mAAbs) – OR2, OR5 and Syn 2H‐11 – with the ability to bind subsets of murine T cells, including the ovalbumin‐specific DO‐11.10 clone. These antibodies did not induce apoptosis in vitro , but prevented interleukin‐2 (IL‐2) production by antigen‐specific T cells. These findings suggest an immunomodulatory function for NAAbs to TCR V‐region epitopes and serve as the foundation for testing human anti‐TCR mAAbs in animal models with the eventual goal of using them as therapeutic agents in human disease.