Abstract
This chapter summarizes the evidence regarding the genetic mechanisms of Mta transmission and the class I nature of the surface antigen. By far the most intriguing aspect of maternally transmitted antigen (Mta) is its strict maternal inheritance. It is because of unawareness of any other cell surface antigen in metazoa that is inherited in this manner. Although the conclusive experiments have yet to be completed, it is thought that the evidence for mitochondrial control of Mta phenotype is rather persuasive. Mta is defined by cytotoxic T-lymphocyte (CTL) recognition; to date no antibodies to Mta have been reported. Mta disparity also induces skin graft rejection as well as weak secondary mixed lyinphocyte responses. Restriction enzyme polymorphism analysis and transfer of mitochondria via cell fusion indicate that the genetic element controlling the Mta polymorphism is probably located within mitochondria.
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