Decrease of LFA-1 is associated with upregulation of TGF-beta in CD4(+) T cell clones derived from rats nasally tolerized against experimental autoimmune myasthenia gravis.

Tolerance to experimental autoimmune myasthenia gravis by nasal administration of microgram amounts of acetylcholine receptor (AChR) has been reported. To elucidate the mechanisms behind tolerance induction via the respiratory tract and the involvement of CD4(+) T cells, we established AChR-specific CD4(+)CD8(-) T cell clones from nasally tolerized rats. Nasal tolerance decreased leukocyte function-associated antigen-1 (LFA-1) expression in CD4(+) T cells from tolerized rats. There was no difference between nasally tolerized and control rats in expression of intercellular adhesion molecule-1. The levels of transforming growth factor-beta (TGF-beta) mRNA-expressing cells were upregulated in CD4(+) T cell clones after tolerance induction. These findings suggest that decreased LFA-1 expression in CD4(+) T cells contributes to reduction of the infiltration of inflammatory CD4(+) T cells, while upregulated TGF-beta may inhibit lymphocyte functions. Copyright 1998 Academic Press.