Compromised melanocyte survival due to decreased suppression of CD4 & CD8 resident memory T cells by impaired TRM-regulatory T cells in generalized vitiligo patients.

Regulatory T cells (Tregs) are involved in the suppression of activated T cells in generalized vitiligo (GV). The study was aimed to investigate resident memory (TRM)-Tregs and antigen-specific Tregs' numbers and functional defects in 25 GV patients and 20 controls. CD4 & CD8 TRM cell proliferation was assessed by BrDU assay; production of IL-10, TGF-β, IFN-γ, perforin and granzyme B were assessed by ELISA and enumeration of TRM cells was done by flowcytometry.

Salt-tolerant bacteria enhance the growth of mung bean ( L.) and uptake of nutrients, and mobilize sodium ions under salt stress condition.

Salinity is one of the significant abiotic stresses that exert harmful effects on plant growth and crop production. It has been reported that the harmfulness of salinity can be mitigated by the use of salt-tolerant plant growth-promoting (PGP) bacteria. In this study, four bacteria were selected from a total of 30 cultures, based on salt-tolerant and PGP properties.

Emerging role of Tissue Resident Memory T cells in vitiligo: From pathogenesis to therapeutics.

Vitiligo is an acquired depigmenting disorder which affects both skin and mucous membranes and autoimmunity has been strongly suggested to play a role in loss of melanocytes. The recurrence of skin macules at the same sites where they were observed prior to the treatment, suggests the existence of Tissue Resident Memory T cells (TRMs) that persist within the skin or peripheral tissues with a longer survivability. Emerging studies have shown that reactivation of these skin TRMs results into autoreactive TRM cells in various autoimmune diseases including vitiligo.

Pathophysiology and recent therapeutic insights of sickle cell disease.

Sickle cell disease (SCD) is an autosomal recessive blood disorder which occurs due to point mutation in the β-globin chain of hemoglobin. Since the past decades, various therapies have been put forth, which are based on obstructing pathophysiological mechanisms of SCD including inhibition of Gardos channel and cation fluxes which in turn prevents sickle erythrocyte destruction and dehydration. The pharmacological approaches are based on the mechanism of reactivating γ-globin expression by utilizing fetal hemoglobin (HbF)-inducing drugs such as hydroxyurea.