Bacillus subtilis-derived-exopolysaccharide halts depigmentation and autoimmunity in vitiligo.

Vitiligo has a complex multifactorial etiology involving a T-cell mediated autoimmune response to cutaneous melanocytes. Microbial dysbiosis has been assigned a contributing role in vitiligo etiology. Treating vitiligo can be a challenging task and finding novel treatment approaches is crucial.

Increased splicing of CXCR3 isoform B (CXCR3B) by impaired NRF2 signaling leads to melanocyte apoptosis in active vitiligo.

Apoptotic melanocytes (MCs) may release neoantigenic epitopes preceding epidermal infiltration by autoreactive CD8 T cells in early vitiligo. However, the mechanism by which vitiligo MCs are prone to apoptosis under oxidative stress remains elusive. Pro-apoptotic receptor C-X-C motif chemokine receptor 3 isoform B (CXCR3B) is critical for inducing MC apoptosis in the inflammatory microenvironment of lesional vitiligo skin.

Decreased Peripheral Blood Natural Killer Cell Count in Untreated Juvenile Dermatomyositis Is Associated with Muscle Weakness.

Juvenile Dermatomyositis (JDM) is the most common inflammatory myopathy in pediatrics. This study evaluates the role of Natural Killer (NK) cells in Juvenile Dermatomyositis (JDM) pathophysiology. The study included 133 untreated JDM children with an NK cell count evaluation before treatment.

Vitiligo: advances in pathophysiology research and treatment development.

The autoimmune condition vitiligo, characterized by skin depigmentation, presents challenges for effective treatment design, with Janus kinase (JAK) inhibitors and other repurposed drugs offering a promising strategy for symptom management. This review explores advantages and shortcomings of current therapies, while presenting the urgent need for further innovative approaches. We emphasize the growing understanding of autoimmune involvement in vitiligo, highlighting several novel treatment avenues including relieving melanocyte stress, preventing dendritic cell activation, halting T cell migration, and suppressing inflammation and autoimmunity.