Melanocyte-specific cytotoxic T lymphocytes in patients with rhododendrol-induced leukoderma

Fujiyama, Toshiharu; Ikeya, Shigeki; Ito, Taisuke; Tatsuno, Kazuki; Aoshima, Masahiro; Kasuya, Akira; Sakabe, Jun‐ichi; Suzuki, Takahiro; Tokura, Y.

doi:10.1016/j.jdermsci.2015.01.017

Cited by 20 publications

(22 citation statements)

References 10 publications

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“…Histology of rhododendrol-induced lesions revealed a significant reduction of melanocytes, melanin incontinence, and an increased infiltration of T cells 42, 75 . Patients also had more melanocyte-specific CD8+ T cells in their blood compared to controls 76 , suggesting that these chemically-induced melanocyte changes activated an autoimmune response that has been observed in conventional vitiligo patients as well 77–79 .…”

Section: Mechanism Of Chemical-induced Vitiligomentioning

confidence: 88%

Chemical-Induced Vitiligo

Harris

2017

Dermatologic Clinics

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Synopsis Chemical-induced depigmentation of the skin has been recognized for over 75 years, first as an occupational hazard but then extending to those using household commercial products as common as hair dyes. Since their discovery, these chemicals have been used therapeutically in patients with severe vitiligo to depigment their remaining skin and improve their appearance. The importance of recognizing this phenomenon was highlighted during an outbreak of vitiligo in Japan during the summer of 2013, when over 16,000 users of a new skin lightening cosmetic cream developed skin depigmentation at the site of contact with the cream and many in remote areas as well. Depigmenting chemicals appear to be analogs of the amino acid tyrosine that disrupt melanogenesis and result in autoimmunity and melanocyte destruction. Because chemical-induced depigmentation is clinically and histologically indistinguishable from non-chemically induced vitiligo, and because these chemicals appear to induce melanocyte autoimmunity, this phenomenon should be known as “chemical-induced vitiligo”, rather than less accurate terms that have been previously used.

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Section: Mechanism Of Chemical-induced Vitiligomentioning

confidence: 88%

Chemical-Induced Vitiligo

Harris

2017

Dermatologic Clinics

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“…1,2 Until recently, the pathogenesis of RIL has been discussed in terms of biochemical, cell biological, and immunological aspects. [2][3][4][5][6][7][8][9][10][11][12] Histopathological and immunohistochemical studies showed basal hypo-pigmentation, melanin incontinence, and a decrease in the number of melanocytes in RIL. 2,10 However, the ultrastructural characteristics of RIL have not been fully elucidated.…”

Section: Introductionmentioning

confidence: 98%

“…It is difficult to clinically distinguish RIL from vitiligo, an auto‐immune disorder targeting melanocytes . Until recently, the pathogenesis of RIL has been discussed in terms of biochemical, cell biological, and immunological aspects . Histopathological and immunohistochemical studies showed basal hypo‐pigmentation, melanin incontinence, and a decrease in the number of melanocytes in RIL .…”

Section: Introductionmentioning

confidence: 99%

Leukoderma induced by rhododendrol is different from leukoderma of vitiligo in pathogenesis: A novel comparative morphological study

et al. 2018

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Background Rhododendrol (rhododenol), an inhibitor of tyrosinase activity, is used as a skin‐whitening component. Many cases of leukoderma after the application have been reported, termed rhododenol‐induced leukoderma (RIL). The aim of this study was to clarify the pathogenesis of RIL morphologically through comparison with vitiligo. Methods We examined 14 cases of RIL and 15 cases of vitiligo using routine histopathology and immunohistochemistry. Thirteen cases of RIL, six cases of vitiligo and specimens of the RIL mouse model were evaluated by electron microscopy. Results There were common findings in RIL and vitiligo at the light‐microscopic level: (a) vacuolar changes in the dermo‐epidermal junction, (b) melanophages in the papillary dermis, (c) perifollicular lymphocyte infiltration, (d) loss or decrease of basal melanin pigment and (e) decrease of melanocytes in the lesions. The ultrastructural observations showed specific findings of RIL: (a) remaining melanocytes in depigmented lesions, (b) inhomogeneous melanization in melanocytes and (c) degenerated melanosomes in melanocytes. Some of the findings were observed in a RIL mouse model. Furthermore, it is notable that cell organelles of melanocytes were intact in our RIL cases. Conclusion Morphological changes of RIL targeting melanosomes in melanocytes without degeneration of organelles reflect the reversible clinical course of most cases.

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“…The JAK–signal transducer and activator of transcription 1 (STAT1)–C‐X‐C motif chemokine 10 (CXCL10) pathway appears to be involved in the pathogenesis of autoimmune vitiligo, blocking this pathway by JAKi suppressing the recruitment of autoreactive T cells to the skin . RD‐induced vitiligo seems to be primarily caused by cellular stress to melanocytes; however, previous studies have suggested that an activated autoimmune response may also be involved in its pathogenesis . We aimed to investigate whether the JAKi tofacitinib may be effective for RD‐induced vitiligo.…”

mentioning

confidence: 99%

“…The pathogenesis of RD‐induced vitiligo primarily occurs due to the cytotoxicity and ER stress caused by RD metabolites to melanocytes, which leads to apoptosis; however, Melan‐A‐specific cytotoxic T cells are frequently seen in patients with RD‐induced vitiligo, suggesting that an autoimmune mechanism is also responsible for pathogenesis. In addition, approximately 5% of RD‐induced vitiligo patients develop the lesion on remote skin areas, which also suggests the possible transition from RD‐induced vitiligo to autoimmune vitiligo.…”

mentioning

confidence: 99%