The role of major histocompatibility complex molecules in luteal function

Introduction One of the amazing features of the corpus luteum (CL) is the rapidity with which a very heterogeneous population of cells becomes organized into a functional unit. These diverse cells then communicate both directly and through paracrine mediators to facilitate the steroidogenic function and also the transient nature of the CL. Once the hormonal regulators of luteal function and demise (for example, LH and prostaglandin F2α) had been clearly delineated, considerable effort in the late 1970s and 1980s was spent characterizing the morphological and functional characteristics of the large and small steroidogenic cells. This was followed in the 1990s by increased interest in the roles that nonsteroidogenic cells, including endothelial cells, fibroblasts, pericytes and immune cells, might have in luteal function. It is now thought that the nonsteroidogenic cells are very active participants in regulating the functional capacity and lifespan of the CL. These cells communicate with the steroidogenic cells through the paracrine signaling molecules that they produce, and also through direct cell contacts. One form of direct cellcell signaling that may serve to activate resident immune cells is major histocompatibility complex (MHC) molecule-dependent interaction between luteal cells with T lymphocytes. Expression of MHC molecules, and recognition of antigenic peptides presented in the context of MHC molecules, serves as a means to regulate the activation of T lymphocytes, thus controlling cytokine production and/or cytolysis.