Unraveling the relation between vitiligo, Interleukin 17, and serum amyloid A

Abstract

The exact etiopathogenesis of vitiligo is still a matter of debade. The development of white macules is the clinical hallmark of vitiligo due to the selective loss of melanocytes. The prevalence of the disease is around 0.5-1.0% worldwide. 1 Vitiligo may be a psychologically distressing condition, especially in people with darker skin because it is more evident on them. It seems to be genetically transmitted in a polygenic/multifactorial way. It has been suggested that immunological factors, oxidative stress, and/or sympathetic neurogenic disruption are the etiology; however, this is still up for debate. 2

Serum amyloid A facilitates expansion of CD4+ T cell and CD19+ B cell subsets implicated in the severity of myasthenia gravis patients

“…The role of SAA in autoimmunity is underscored by data showing that SAA are associated with clinical severity and disease susceptibility. Several authors, comparing serum SAA levels between healthy and diseased individuals, showed an increase in SAA concentration during autoimmune diseases (Ahmed et al., 2022; Shen et al., 2015; Wang et al., 2020; Yoon et al., 2020). Notably, SAA can act directly on T cells and promote Th17 cell programming and response amplification, which revealed in inflammatory bowel disease (IBD) and experimental autoimmune encephalomyelitis (EAE) models (Lee et al., 2020).…”