Vitiligo is a disease caused by the acquired depletion of melanocytes and/or melanocyte precursor cells in response to genetic and environmental factors, resulting in depigmentation of the entire body. It is roughly divided into segmental and non-segmental vitiligo, and it has been found that abnormalities of melanocytes themselves and dysregulation of autoimmune responses to melanocytes are greatly involved in the pathology of non-segmental vitiligo.Segmental vitiligo pathology is largely unknown; however, it has been suggested that it may be caused by skin or melanocyte mosaicism. Treatments for vitiligo include topical therapy, ultraviolet therapy, and surgical transplantation, and it is extremely important to correctly understand the pathology to perform optimal treatment. In recent years, the development of vitiligo treatments using Janus kinase (JAK) inhibitors has progressed rapidly. We herein outline the latest pathology of vitiligo, from general vitiligo treatment to the progress of clinical trials using JAK inhibitors, along with what clinicians should consider in archiving precision medicine, including my own ideas thereon.

BACKGROUND: Peculiar erythema known as annular erythema associated with Sjogren's syndrome (AESS) can be differentiated from autoimmune annular erythema and subacute cutaneous lupus erythematosus, both clinically and histologically. However, there are no detailed investigations on immune competent cells infiltration. OBJECTIVE: Preferential infiltration of interleukin-17-producing T helper (Th17) cells and regulatory T (Treg) cells into the labial salivary gland is reported to play a role in maintaining mucoepithelitis in patients with Sjogren's syndrome. In this study, we evaluated Th17 and Treg cell infiltration into the lesional skin of AESS. METHODS: We analyzed the numbers and infiltration patterns of Th17 and FoxP3 (+) Treg cells in seven cases of AESS using immunohistochemistry. Seven patients with systemic lupus erythematosus (SLE), atopic dermatitis (AD) and psoriasis vulgaris (PV), which are representatives of Th17 cell-involved skin disorders, were enrolled as disease controls. RESULTS: Periappendageal and epidermal changes, such as follicular plugging and liquefaction, were evident in the annular erythema of SLE, not AESS, tissue samples. In AESS tissue samples, dense perivascular and periappendageal infiltration of lymph cells was observed in the middle-to-deep dermis, as previously described, in contrast to the superficial infiltration pattern observed in both AD and PV samples. While the total number of infiltrated lymphocytes was similar between AESS and SLE tissue samples, Th17 cells were found to be preferentially infiltrated in the middle-to-deep dermis in AESS samples. CONCLUSION: These results suggest that an increased number and distribution of infiltration of Th17 cells is a preferential feature of AESS, rather than a characteristic feature of annular erythema of SLE.
Dermatitis, Atopic ; Dermis ; Erythema* ; Humans ; Immunohistochemistry ; Interleukin-17* ; Lupus Erythematosus, Cutaneous ; Lupus Erythematosus, Systemic ; Lymphocytes ; Psoriasis ; Salivary Glands ; Sjogren's Syndrome* ; Skin ; T-Lymphocytes, Helper-Inducer* ; T-Lymphocytes, Regulatory* ; Th17 Cells