Mls-like endogenous superantigens have been reported to be unique, differing from conventional antigens in the T cell receptor (TCR) requirements for their recognition, in the signal transduction events which they elicit in T cells, and in the identity of the stimulatory ligand. This review describes recent findings indicating that TCR V alpha as well as V beta products play a role in Mls recognition. Data are also summarized which indicate that T cell recognition of Mls leads to increased intracellular [Ca2+] and phosphatidyl inosotol hydrolysis. Finally, genetic linkage between mouse mammary tumor virus (MMTV) proviruses and endogenous superantigens is analyzed, and the possible role of non-MMTV products is examined.