No abstract

Background Multiple sclerosis (MS) is an autoimmune inflammatory disease of the central nervous system (CNS) that T cells become autoreactive by recognizing CNS antigens. Both innate and adaptive immune systems are involved in the pathogenesis of MS. In recent years, the impact of innate immune cells on MS pathogenesis has received more attention. CD56bright NK cells, as an immunoregulatory subset of NK cells, can increase the production of cytokines that modulate adaptive immune responses, whereas CD56dim NK cells are more active in cytolysis functions. These two main subsets of NK cells may have different effects on the onset or progression of MS. Invariant NKT (iNKT) cells are other immune cells involved in the control of autoimmune diseases; however, variant NKT (vNKT) cells, despite limited information, could play a role in MS remission via an immunoregulatory pathway. Aim We aimed to evaluate the influence of MS therapeutic agents on NK and NKT cells and NK cell subtypes. Materials and Methods The possible mechanism of each MS therapeutic agent has been presented here, focusing on the effects of different disease‐modifying therapies on the number of NK and NKT subtypes. Results Expansion of CD56bright NK cells, reduction in the CD56dim cells, and enhancement in NKT cells are the more important innate immune cells alterations following the disease‐modifying therapies. Conclusion Expansion of CD56bright NK cells or reduction in the CD56dim cells has been associated with a successful response to different treatments in MS. iNKT and vNKT cells could have beneficial effects on MS improving. It seems that they are enhanced due to some of MS drugs, leading to disease improvement. However, a reduction in the number of NKT cells could be due to the adverse effects of some of MS drugs on the bone marrow.

Background and aims Endometrial cancer (EC) and breast cancer (BC) are prevalent in women. Visfatin is an adipokine that, in addition to being involved in metabolism and inflammation, may also be interested in carcinogenesis. Visfatin measurement in cancer patients has shown that visfatin levels in cancer patients differed from those in healthy subjects. Various studies have shown that the level of visfatin is increased in people within EC and BC, and this difference has a significant relationship with prognosis. Methods A comprehensive search of related articles from PubMed, Scopus, Web of Science, and the Google Scholar database was done by November 2021. Eligible articles measured visfatin levels in patients with breast cancer and EC. After selecting the eligible studies, the data were extracted and analyzed using the random effect method. Results Given the effect size and the confidence interval obtained, the total level of visfatin in cancer patients was different from that in healthy individuals, and this difference was statistically significant. However, the difference in visfatin levels in patients with breast cancer was much more significant than in patients with EC compared to the control group. Conclusions Due to the significant increase in visfatin levels in these patients, visfatin may be a potential prognostic factor in breast and ECs. Visfatin levels in cancer patients differed from those in healthy subjects, and this difference was also statistically significant ( p ‐values = 0.00). Visfatin levels also differed between breast cancer patients and healthy individuals, which was statistically significant ( p ‐values = 0.00). The difference in visfatin levels between patients with EC and healthy subjects was statistically significant ( p ‐values = 0.047).