Genetic control of T cell activation induced by Mycoplasma arthritidis

Abstract

At least three genes are now known to influence T-lymphocyte activation induced by the soluble mitogen derived from Mycoplasma arthritidis (MAM). The I-E region of the murine major histocompatibility complex (MHC) codes for the synthesis of the E alpha chain of the I-E molecule, which acts as a receptor for MAM. Mouse, rat and human E alpha molecules have a similar structure, and lymphocytes from all of these species can be activated by MAM. However, lymphocytes from the BN rat, which also express this molecule, fail or respond only weakly to MAM and lectin mitogens due to the influence of a non-MHC gene(s). The RIIIS mouse strain also expresses the E alpha receptor site for MAM, but possesses a recessive non-MHC gene(s) that is associated with an inability of lymphocytes to respond to MAM without influencing their responses to lectin mitogens. There is evidence that in the BN rat and the RIIIS mouse there is a defect in T cell interactions with the mitogen/accessory cells complex. Evidence is also presented that T-lymphocyte activation in vivo may predispose mice to the toxic and necrotizing properties of viable M. arthritidis.