Expression of Major Histocompatibility Complex Antigens on the Bovine Corpus Luteum during the Estrous Cycle, Luteolysis, and Early Pregnancy1

Abstract

Treatment of cultured bovine luteal cells with the cytokine, interferon-gamma, induces the expression of Class II major histocompatibility complex antigens (MHC Ags). To determine if Class II MHC Ags are present on the CL in vivo and if the degree of Ag expression changes during luteal life span, bovine corpora lutea were obtained on Day 6, Days 10-12, and Day 18 of the estrous cycle and MHC Ag expression was evaluated via indirect immunofluorescence. Flow cytometry was used to determine the percentage of MHC Ag-positive cells on cell populations distinguished by cell size and intracellular density. Minimal Class II MHC Ag expression was detected on Day 6 CL (approximately 25%), which consisted primarily of smaller cells. The midcycle and late CL consisted of these small cells (SC) and two populations of large cells that differed in intracellular density, or right-angle light scatter. In midcycle CL, few (less than 25%) SC or large, dense cells (LDC) expressed the Class II MHC Ag whereas a high percentage (75%) of the large, less-dense cells (LLDC) were Class II MHC Ag-positive. Class II MHC Ag expression remained negligible on the LDC of the Day 18 CL; however, there was an elevation in the percentage of SC and LLDC expressing Class II Ag (p less than 0.05). To determine if Class II MHC Ag expression also varied with different functional states of the CL, bovine CL were collected after prostaglandin (PG) F2 alpha-induced regression and on Day 18 of early pregnancy. When luteolysis was allowed to progress in vivo, the percentage of Class II MHC Ag-positive cells was increased in all cell populations (p less than 0.05). Class II MHC Ag expression was significantly lower (p less than 0.05) on the three cell populations comprising the CL of pregnancy as compared to the Day 18 cyclic CL. It is hypothesized that enhanced expression of Class II MHC Ags on the late CL and during PGF2 alpha-induced regression may potentiate immune response mechanisms for luteolysis.