Neuro-Immuno-Endocrine Processes in Vitiligo Pathogenesis

Abstract

Vitiligo is a cutaneous disorder of depigmentation, clinically characterized by well-demarcated, white macules of varying size and distribution. It can affect up to 2 percent of the population, especially younger ages. In spite of recent findings implicating genetic, immune and oxidative stress factors, the exact pathogenesis of vitiligo remains obscure. Here, we briefly discuss the prevailing theories, and offer new suggestions that could explain in part the damage of melanocyte in the vitiliginous lesions. Our emerging hypothesis is that neuropeptides released from peripheral nerve endings could synergize with new cytokines to adversely affect melanocyte function and viability. These may include corticotropin- releasing hormone (CRH) and neurotensin (NT), as well as interleukin 33 (IL-33) and thymic stromal lymphopoietin (TSLP). Such interactions could serve the basis for further research, possibly leading to new treatments.

Psychoneuroimmunoendocrinology: clinical implications

“…Based on the pathophysiological mechanisms described above, the psychoneuroimmunoendocrine axis has been related to neuropsychiatric diseases such as depression [4, 55–57] and schizophrenia [56, 58–61], metabolic syndrome [62, 63], rheumatologic and autoimmune diseases [64–72], irritable bowel syndrome [73, 74], periodontal disease [75, 76] and neoplastic diseases [62, 77], and these relationships warrant significant attention. Psychoneuroimmunology represents the challenge of health professionals to achieve multidisciplinary management of each of these pathologies.…”

Cutaneous expression of thymic stromal lymphopoietin (TSLP) in vitiligo patients: a case‐control study

“…Increasing evidence indicates that molecules such as IL‐9, IL‐33, and TSLP are released following a number of insults and can activate many immune cells, especially mast cells. Given the recent report of the increased number of mast cells in the center of the vitiliginous skin, it is attractive to explore the possible associations between these inflammatory cytokines that could contribute to the initiation and/or the progression of the disease, either through or independently of mast cells …”

“…Given the recent report of the increased number of mast cells in the center of the vitiliginous skin, it is attractive to explore the possible associations between these inflammatory cytokines that could contribute to the initiation and/or the progression of the disease, either through or independently of mast cells. 9 An interesting genetic fact was the identification of a polymorphism for the TSLP gene-847 C allele > T allele. This polymorphism causes decrease in the expression of TSLP messenger RNA (mRNA) and was found to be associated with generalized vitiligo.…”

Druggable Vitiligo Genome: A Fast Track Approach to Take the Genome Wide Association to the Clinic

“…In the recent years, numerous theories have been put forward. 1,[5][6][7][8][9][10][11][12] Current evidence encompasses four main theories: the autoimmune hypothesis, the neural hypothesis, the self destruct hypothesis and the growth factor defect hypothesis. 13 However, none of these have been conclusively proven to date.…”