Передовые биомедицинские исследования и инновации

Menstrual blood derived stromal stem cells augment CD4+ T cells proliferation

Alireza Ghanavatinejad, Mehdi Aleahmad, Mahmood Bozorgmehr, Mohammad-Reza Shokri, Shohreh Nikoo, Maryam Tavakoli, Somaieh Kazemnejad, Fazel Shokri and Amir-Hassan Zarnani

Introduction: One of the most controversial issues in reproductive biology is dealing with the fact that a fully functional immune system in women should simultaneously fight off the invading pathogens and tolerate semi-allograft fetus throughout the pregnancy. Indeed, a successful pregnancy is supposed to remain unresponsive to paternal antigens originating from semi-allograft fetus. Thus far, extensive attempts and studies have been performed to unravel immunosuppressive mechanisms involved in immunological tolerance of gestation. Endometrium undergoes immunological changes to estab- lish tolerance during the onset of pregnancy. Along with gestation initiation, such immune cells as Natural Killer cells (NKs), monocytes, Dendritic Cells (DCs) and T cells are recruited to the endometrium. The phe- no type of decidual immune cells changes in a way to cooperate with tolerance. Selected NK cells, for in-position, change into decidual NK cells (dNK) with a decreased cytotoxic and expanded secretary movement 1-3. Macrophage and NK cells together initiate tolerogenic DCs (tDCs) 4, which fundamentally advance Treg differentiation. Nevertheless, it has been reported that depleting Tregs causes only a 10% fetal loss in the first pregnancy of mice 5. Indeed, there is evidence that Fas (First apoptosis signal), Indoleamine 2,3-dioxygenase (IDO) and Programmed Death-Ligand 1 (PD-L1) suppress fetus antigen-specific effector T cells 6-8, but immuno- tolerance is not interrupted even if one of these factors is absent in allogeneic mating’s in Ido1−/− or Fasl−/− mice 6,9. Despite the fact that repetition and covering compensatory systems may clarify to a limited extent the before said marvel, one enticing speculation would be immunomodulation at the feto-maternal interface by non-invulnerable cells dwelling in the endometrium.