DESCRIPTION (Adapted from the applicant's abstract): The overall long term objectives are to define the mechanisms by which a mycoplasmal superantigen, MAM, which is derived from Mycoplasma arthritidis, activates lymphocytes and to determine the role of MAM in chronic mycoplasmal disease and in induction of autoimmunity. The specific aims are to study MAM in respect to: 1) Characterization of MAM and its structural and functional relationship with other superantigens: a. to obtain the amino acid sequence of the entire MAM molecule by molecular cloning and to search for sequence homologies with other known proteins to gain insight into the function of MAM and distribution of MAM-like molecules; b. to compare the structure and function of MAM to the Gram positive toxin super-antigens and the M1s self antigens; c. to further define the interaction of MAM with MHC and V beta TCR molecules; d. to obtain expression of MAM in an appropriate host in order to facilitate preparation and increase yields of homogeneous MAM. 2) To develop MAM as a model for microbial-induced modulation of autoimmune diseases using type II collagen-induced arthritis of mice and rats. 3) To determine the role of MAM in Mycoplasma arthritidis-induced arthritis in respect to: a. effect of MAM on acute disease mediated by M. arthritidis; b. effect of fetal or neonatal exposure to M. arthritidis on the T cell repertoire; c. Is chronic arthritis due to a restricted V beta TCR-bearing T cell subset? d. Do MAM or other superantigens play a role in disease chronicity and disease flare ups?