Autoantibodies detected in patients with vitiligo vulgaris but not in those with rhododendrol-induced leukoderma

Arase, Noriko; Tanemura, Atsushi; Jin, Hui; Nishioka, Motomu; Aoyama, Yumi; Oiso, Naoki; Matsunaga, Kayoko; Suzuki, Tamio; Nishigori, Chikako; Kawamura, Tatsuyoshi; Shimizu, Tadamichi; Ito, Akiko; Fukai, Kazuyoshi; Abe, Yuko; Yang, Lingli; Tsuruta, Daisuke; Takeoka, Keiko; Iwatani, Yoshinori; Hidaka, Yoh; Nishida, Makoto; Yamauchi–Takihara, Keiko; Arase, Hisashi; Fujimoto, Manabu; Katayama, Ichiro

doi:10.1016/j.jdermsci.2019.06.009

Cited by 5 publications

(4 citation statements)

References 10 publications

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“…Moreover, although a limited number of patients were analyzed, a significant number of autoantibodies were detected in the serum of patients of vitiligo but not RDL. This suggests that the factors involved in the onset of vitiligo and RDL may differ 30 …”

Section: Mechanism Of Rdl Developmentmentioning

confidence: 99%

“…This suggests that the factors involved in the onset of vitiligo and RDL may differ. 30 In addition, it has recently been reported that the antiprogrammed death 1 antibody, a checkpoint blockade drug, causes vitiligo, possibly owing to an enhanced autoimmune response to melanocytes. Thus, additional pathways may also need to be considered for the immunological aspects of RDL.…”

Section: Involvement Of the Immune System In Rd-induced Melanocyte Lossmentioning

confidence: 99%

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Rhododendrol‐induced leukoderma update II: Pathophysiology, mechanisms, risk evaluation, and possible mechanism‐based treatments in comparison with vitiligo

Inoue

Katayama

Suzuki

et al. 2021

The Journal of Dermatology

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A small proportion of individuals utilizing cosmetics containing rhododendrol developed leukoderma with various pathological conditions, in some cases indistinguishable from vitiligo. In this review, we investigate and evaluate the major considerations for developing rhododendrol‐induced leukoderma based on data from original or review articles published in the literature to provide a wide range of information regarding the pathophysiology, mechanisms, risk evaluation, and possible mechanism‐based treatments. We compile and discuss the latest information, including data related to the cytotoxicity of rhododendrol, cytoprotective functions, and involvement of the immune system, and consider the possibility of novel treatments based on the differences between individual patients and on the mechanism underlying the onset of the condition. Understanding the pathophysiology of rhododendrol‐induced leukoderma helps not only elucidate the mechanisms of non‐segmental vitiligo onset and progression, but also suggests prevention and treatment.

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Section: Mechanism Of Rdl Developmentmentioning

confidence: 99%

Section: Involvement Of the Immune System In Rd-induced Melanocyte Lossmentioning

confidence: 99%

Rhododendrol‐induced leukoderma update II: Pathophysiology, mechanisms, risk evaluation, and possible mechanism‐based treatments in comparison with vitiligo

Inoue

Katayama

Suzuki

et al. 2021

The Journal of Dermatology

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“…Majority of the autoimmune disorders occur due to the development of autoantibodies against host cells. Studies on vitiligo, have shown a similar phenomenon, where circulating autoantibodies like anti-thyroid peroxidase (anti-TPO) 41 , IgA 42 and others that are against melanocytes were found to be high in the serum . 43,45 A recent meta-analysis on the same, showed that people with vitiligo had higher concentrations of anti-thyroglobulin (ATG) antibodies, antinuclear antibodies (ANA), anti-gastric parietal cell antibodies (AGPCA) and anti-adrenal antibodies compared to healthy individuals; providing an insight that vitiligo can also lead to development of other complex autoimmune disorders 46. There is no clarity on the factors that induce the formation of these autoantibodies.…”

Section: Role Of Autoantibodiesmentioning

confidence: 83%

Molecular factors in the development of vitiligo

Venkatesh¹,

Mendez²,

Rajshekhar³

et al. 2019

JCBS

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Vitiligo is a chronic autoimmune disease, caused due to selective destruction of melanocytes. It is characterized by depigmentation of skin. The mechanisms that underlie this phenomenon has not been clearly understood. Therefore, the aim of this review was to collate all the emerging information regarding the involvement of molecular components in vitiligo pathogenesis. Initial surveys suggested that certain chemicals were responsible for causing this skin disease. Recent genetic studies like twin studies show that vitiligo arises due to hereditary factors. Certain predisposing risk variants have been identified through can-didate gene studies and Genome-Wide Association Studies (GWAS). Skin biopsies and peripheral blood of vitiligo patients have revealed the presence of melanocyte targeting autoantibodies, increased T-cells and high levels of inflammatory cytokines, indicating that both humoral and cellular immunities play a major role in selective destruction of melanocytes. In addition to this, studies have shown the association of vitiligo with other autoimmune diseases, implicating that complications of other autoimmune diseases could lead to the development of vitiligo. Further research is required to understand the immune pathway of vitiligo and its commonness with other autoimmune disorders. This would help in tackling the disease therapeutically. Keywords: Vitiligo, Genetics, Autoimmunity, Human Leukocyte Antigen, Cytokines

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“…Chemical leukoderma, however, does not share the autoimmunity changes (e.g., anti-TYRP1 antibody) as it occurs in vitiligo, despite promoting direct damage to melanocytes. 101 …”

Section: Vitiligo Induced By Chemical Agentsmentioning

confidence: 99%