Expression of major histocompatibility complex antigens on the bovine corpus luteum during the estrous cycle, luteolysis, and early pregnancy.

1991 
Treatment of cultured bovine luteal cells with the cytokine, interferon.y, induces the expression of Class II major histocompatibility complex antigens (MHC Ags). To determine if Class U MHC Ags are present on the CL in vlvo 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 Day6 CL (-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 CI, few (<25%) SC or large, dense cells (LDC) expressed the Class U MHC Ag whereas a high percentage (75%) of the large, less-dense cells (LLDC) were Class II MHC Ag-positive. Class II MUC Ag expression remained negligible on the WC of the Day 18 CL; however, there was an elevation in the percentage of SC and LLDC expressing Class II Ag (p < 0.05). To determine if Class ll MHC Ag expression also varied with different functional states of the Cl, bovine CL were collected after prostaglandin (PG) Fas-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 <0.05). Class U MHC Ag expression was significantly lower (p < 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 PGF,�-induced regression may potentiate immune response mechanisms for luteolysis.
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