Non-classical major histocompatibility complex class makes a crucial contribution to reproduction in the dairy cow.

نویسندگان

  • Lei Shu
  • Xiuli Peng
  • Shen Zhang
  • Ganzhen Deng
  • Yue Wu
  • Mingyue He
  • Beibei Li
  • Chengye Li
  • Kechun Zhang
چکیده

The aim of this study was to evaluate the effect of classical and non-classical major histocompatibility complex (MHC) on the reproduction in the dairy cow. Nine pairs of MHC-I genes were chosen according to their homology and possible function, and their transcription levels in maternal peripheral blood mononuclear cells (PBMCs) from all three trimesters and transcription levels in fetal tissues were compared to evaluate their contributions to cattle reproduction. The results showed that three non-classical genes were variably expressed in PBMCs of pregnant cows. MICB was downregulated in the first and second trimesters (P<0.05), but recovered back to the level in replacement heifers in the last trimester (P>0.05). BoLA-NC1* was upregulated in the first and last trimesters (P<0.001) but no different in the second trimester (P>0.05). BoLA-NC3* was upregulated in all trimesters (P<0.001). On the other hand, MICB was upregulated in fetal ear tissues (P<0.001), and BoLA-NC1* was almost silent in both fetal placenta and ear tissues (P<0.001); however, BoLA-NC3* was upregulated in both the fetal placenta and ear tissues (P<0.001). These results suggested that non-classical gene BoLA-NC1* increased maternal immunity against the fetus, which was inhibited by BoLA-NC3*. BoLA-NC3* also inhibited fetal autoimmunity. Apoptosis of the fetal placenta could reduce itself expressing MICB, and upregulated expression of MICB in ear tissues was favorable for the fetus to escape autoimmunity. On the other hand, downregulated expression of MICB in the fetal placenta allows for placental decoherence from the maternal placentome, which was beneficial to fetus delivery. Although classical genes were expressed differentially, their effects were restricted because of heavy chain deficiency.

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عنوان ژورنال:
  • The Journal of reproduction and development

دوره 58 5  شماره 

صفحات  -

تاریخ انتشار 2012