Expression of major histocompatibility complex class II but not of CD8 molecules by lectin-stimulated peripheral CD4+ T cells in LEC mutant rats

Abstract

LEC rats show a congenital maturational arrest from CD4+8+ to CD4+8- but not to CD4-8+ cells in the thymus. However, some CD4+ cells exist in peripheral lymph nodes. In normal F344 rats, a part of CD4+ T cells expressed CD8 molecules upon concanavaline A (Con A) stimulation. The percentage of CD4+8+ cells and the level of CD8 expression in F344 rat CD4+ cells were enhanced by the glucocorticoid hormone dexamethasone. In contrast, although LEC rat CD4+ cells induced DNA synthesis normally upon Con A stimulation, expression of CD8 was significantly reduced. Furthermore, addition of dexamethasone did not restore the inhibition of CD8 expression. However, LEC rat CD4+ cells could induce CD8 expression, when stimulated by T cell receptor (TCR) cross-linking with anti-TCR monoclonal antibody, suggesting that the TCR-mediated signal is normally transduced in LEC rat CD4+ cells. On the other hand, LEC rat CD4+ cells showed normal expression of major histocompatibility complex (MHC) class II antigens, when stimulated by either Con A or TCR cross-linking, indicating that signals for the induction of MHC class II expression are normal in LEC rat CD4+ cells. Activation of peripheral CD4+ cells has been reported to induce simultaneous expression of CD8 and MHC class II molecules in rats. However, our results using LEC rat CD4+ cells suggest that Con A-induced signaling pathways for CD8 and MHC class II expression can be separable.