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, specific and effectual therapeutic protocols for patients with unexplained RPL may be well established.