Murine experimental autoimmune thyroiditis (EAT) is a T-cell-mediated disease, but the T cell receptor (TCR) Vβ gene usage in pathogenesis has not been well delineated. One approach is to utilize bacterial superantigens, such as staphylococcal enterotoxin (SE) A and B, to stimulate known sets of TCR Vβ families in mouse thyroglobulin (mTg)-primed cells for thyroiditis transfer. Our previous use of SEB to activate mTg-primed cells led to no thyroiditis transfer, despite a major increase in Vβ8+ T cells. Unlike SEB, SEA activation did transfer thyroiditis. To determine which thyroiditogenic Vβ+ T cells were involved, SEA-activated T cells have now been analyzed. After repeated SEA activation in vitro, both mTg-reactive and thyroiditogenic cells persisted. FACS analysis indicated that most Vβ13+ cells were "large" cells (IL-2R+) and expressed the activation marker, transferrin receptor (CD71). RT-PCR analysis also showed the presence of both Vβ13+ and SEA-reactive Vβ1+ cells. Since our previous analyses by RT-PCR of the thyroid infiltrate after either induction or adoptive transfer have implicated both Vβ13+ and Vβ1+ cells, their activation by SEA to transfer thyroiditis further supports their role.
- Experimental autoimmune thyroiditis
- In vivo animal models
- T lymphocytes
ASJC Scopus subject areas