Conclusion:
The maternal-embryonic interface is well thought-out to be
immunosuppressed so that there is the healthy growth of the
placental-embryonic unit. The profiling of decidual cytokines and
diversity of decidual cells recommends that the in vivo condition is
more complicated. Cytokines are minute protein molecules that perform
multiple functions. They are often derived white blood cells and
described through their immune modulatory actions. The cytokines from
decidua in addition to their immunosuppression role also participate in
the establishment of pregnancy via regulating the invasion of
trophoblasts and modifying the spiral blood arteries. Different
cytokines and chemokines discharged from the decidual as well as
embryonic cells at the time of implantation trigger many signaling
networks between the mother and the embryo. Errors in the development of
decidua during early gestational months result in pregnancy failure or
later gestational complications. The management of RPL in a large
proportion of cases due to the ambiguity of diagnosis is still
undergoing progression. Correction of IL11 signaling in the endometrium
may be one of the potential therapeutic approach for preventing
infertility and miscarriage. Further exhaustive research in reproductive
immunology is required with the aim to explore the detailed contribution
of NK cells and Treg cells along with various cytokines and antigenic
proteins to the etiology of RPL. Once a broad comprehension of the
modulation of the endometrial immune atmosphere due to cytokines is
developed and a molecular clue for the etiology of unexplained RPL is
acquired, new, speciļ¬c and effectual therapeutic protocols for patients
with unexplained RPL may be well established.