Fuller B E, Giraldo A A, Motte R W, Nabozny G H, David C S, Kong Y M
Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, Michigan 48201.
Cell Immunol. 1994 Dec;159(2):315-22. doi: 10.1006/cimm.1994.1317.
In experimental autoimmune thyroiditis (EAT) induced with mouse thyroglobulin (MTg), T cell receptor (TCR) V beta gene usage in the pathogenesis of disease is unknown. We report here studies evaluating V beta 8 gene usage in EAT, as V beta 8+ T cells are reportedly involved in some experimental autoimmune diseases. Spleen cells (SC) from MTg-immunized CBA/J (H-2k) mice were activated in vitro for adoptive transfer into syngeneic recipients. Elimination of V beta 8+ T cells by treating recipients with V beta 8 monoclonal antibody (mAb) following transfer of MTg-activated SC did not reduce disease severity. Conversely. MTg-primed SC were stimulated in vitro with V beta 8 mAb or staphylococcal enterotoxin B, which activates V beta 8+ T cells in CBA/J mice. Neither activated population transferred disease, in contrast to cells activated with MTg. Thus, in MTg-induced EAT, V beta 8+ T cells do not play a major role in pathogenesis.