Abstract
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.
Original language | English (US) |
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Pages (from-to) | 149-157 |
Number of pages | 9 |
Journal | Cellular Immunology |
Volume | 213 |
Issue number | 2 |
DOIs | |
State | Published - Nov 1 2001 |
Keywords
- Autoimmunity
- EAT
- Experimental autoimmune thyroiditis
- In vivo animal models
- SEA
- Superantigens
- T lymphocytes
- Thyroglobulin
- Vβ1
- Vβ13
ASJC Scopus subject areas
- Immunology