Atrophying pityriasis versicolor as an idiosyncratic T cell–mediated response to Malassezia : A case series

Levy, Jonathan M.; Magro, Cynthia M.

doi:10.1016/j.jaad.2016.08.062

Cited by 17 publications

(13 citation statements)

References 17 publications

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“…Several Malassezia metabolites, particularly indirubin and tryptanthrin, are reportedly ligands of the AhR, which stimulates NHKCs to increase the production of CYP1A1 as well as proinflammatory and Th2 cytokines . In addition, Malassezia species indirectly increase MMP activity . We therefore hypothesized that stimulation of NHKCs by Malassezia yeast induces increased production and activity of characteristic MMPs, chemokines and cytokines correlated with the progression of EMPD.…”

Section: Resultsmentioning

confidence: 99%

Malassezia‐derived aryl hydrocarbon receptor ligands enhance the CCL20/Th17/soluble CD163 pathogenic axis in extra‐mammary Paget's disease

Sato

Fujimura

Tanita

et al. 2019

Experimental Dermatology

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Malassezia yeast play a role in the pathogenesis of chronic dermatitis, especially in apocrine areas, by polarizing the local immunologic background to a Th2/Th17 state through aryl hydrocarbon receptor (AhR)-dependent pathways. Extra-mammary Paget's disease (EMPD) is an adenocarcinoma of apocrine origin, and except for cases associated with Malassezia yeast and their metabolites, the lesions typically develop in areas not exposed to environmental material. The purpose of this study was to investigate (a) the immunomodulatory effects of Malassezia metabolites on normal human keratinocytes (NHKCs), focusing on interleukin (IL)-17 and related cytokines/ chemokines (IL-23, IL-36γ, CCL20), (b) the expression of these factors in lesion-affected skin in EMPD and (c) the activation of tumor-associated macrophages (TAMs) by these factors. Malassezia metabolites augmented the expression of cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1), CCL20 and IL-36γ mRNA in NHKCs in vitro. In lesion-affected skin of patients with EMPD, epidermal keratinocytes expressed CYP1A1 and CCL20. In addition, Paget cells expressed CCL20 and IL-23. IL-17-producing cells were distributed adjacent to Paget cells. Compared to healthy donors, patients with EMPD exhibited significantly increased serum levels of soluble (s)CD163, CXCL5, CXCL10 and CCL20. In addition, serum levels of sCD163 decreased significantly following tumor resection. Our study demonstrates a possible mechanism for the development of EMPD involving AhR-mediated signalling by epidermal keratinocytes and RANKL-induced recruitment of Th17 cells and TAMs. K E Y W O R D Saryl hydrocarbon receptor, extra-mammary Paget's disease, Malassezia, proinflammatory cytokines, tumor-associated M2 macrophages

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Section: Resultsmentioning

confidence: 99%

Malassezia‐derived aryl hydrocarbon receptor ligands enhance the CCL20/Th17/soluble CD163 pathogenic axis in extra‐mammary Paget's disease

Sato

Fujimura

Tanita

et al. 2019

Experimental Dermatology

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“…It was postulated that the fungal disruption of the skin barrier allowed greater absorption of the corticosteroid, resulting in atrophic spots . However, typical corticosteroid‐induced atrophy causes a reduction in the dermal collagen with minimal reduction in dermal elastic fibers . This mechanism contradicts pathologic findings reported in previous atrophic TV cases, suggesting this is a predominantly epidermal process with mild superficial papillary dermis involvement; both are secondary to a T H 1‐dominant cell response to the fungus.…”

Section: Discussionmentioning

confidence: 97%

“…Atrophic tinea versicolor (TV) caused by Malassezia furfur was first described in a case report in 1971 . Despite several subsequent case reports, the pathophysiologic mechanism of this uncommon variant remains unclear.…”

Section: Discussionmentioning

confidence: 99%

An adolescent girl with atrophic plaques on her trunk

Robbins

Fischer

DeWitt

et al. 2019

Pediatric Dermatology

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A 12-year-old girl presented for new evaluation and treatment of a progressive truncal rash over the past several years which had been intermittently pruritic. She attempted treatment with overthe-counter antifungals, antidandruff shampoos, and steroid creams with only modest, temporary improvement. Physical exam demonstrated multiple, thin, coalescing, scaly, erythematous plaques on the central chest and upper back. At her initial dermatology visit, she was prescribed triamcinolone 0.1% cream twice daily three times per week along with an emollient twice daily. When seen in follow-up 2 months later, her rash had progressed despite prescribed topical treatments. The family also reported a deeper purple hue to the rash and new truncal acne. On examination, sharply demarcated, focally coalescent, lilac-colored areas with depression to the level of the epidermis and subtle scale were noted on the back, chest, abdomen, flanks, and neck (Figure 1). The upper back and chest also exhibited scattered inflammatory papules and a few pustules.

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“…T cell-responsiveness to Malassezia in such patients was associated with a Th2 response ( 88 ), in line with the classical paradigm of Th2-polarized allergic T cells. GATA3 + T cells were identified in pityriasis versicolor lesions ( 89 ) and likewise Malassezia -specific T cell in allergic dogs were found to be strongly polarized toward a type 2 response ( 82 ). More recently, other T helper cell subsets such as Th17 and Th22 cells have been found enriched in allergic individuals ( 90 , 91 ) as well as in non-allergic immune-mediated skin diseases such as psoriasis ( 92 ).…”

Section: Adaptive Immunity To Malassezia Sppmentioning

confidence: 99%

Host Responses to Malassezia spp. in the Mammalian Skin

Sparber

LeibundGut‐Landmann

2017

Front. Immunol.

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The skin of mammalian organisms is home for a myriad of microbes. Many of these commensals are thought to have beneficial effects on the host by critically contributing to immune homeostasis. Consequently, dysbiosis can have detrimental effects for the host that may manifest with inflammatory diseases at the barrier tissue. Besides bacteria, fungi make an important contribution to the microbiota and among these, the yeast Malassezia widely dominates in most areas of the skin in healthy individuals. There is accumulating evidence that Malassezia spp. are involved in a variety of skin disorders in humans ranging from non- or mildly inflammatory conditions such as dandruff and pityriasis versicolor to more severe inflammatory skin diseases like seborrheic eczema and atopic dermatitis. In addition, Malassezia is strongly linked to the development of dermatitis and otitis externa in dogs. However, the association of Malassezia spp. with such diseases remains poorly characterized. Until now, studies on the fungus–host interaction remain sparse and they are mostly limited to experiments with isolated host cells in vitro. They suggest a multifaceted crosstalk of Malassezia spp. with the skin by direct activation of the host via conserved pattern recognition receptors and indirectly via the release of fungus-derived metabolites that can modulate the function of hematopoietic and/or non-hematopoietic cells in the barrier tissue. In this review, we discuss our current understanding of the host response to Malassezia spp. in the mammalian skin.

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Atrophying pityriasis versicolor as an idiosyncratic T cell–mediated response to Malassezia : A case series

Cited by 17 publications

References 17 publications

Malassezia‐derived aryl hydrocarbon receptor ligands enhance the CCL20/Th17/soluble CD163 pathogenic axis in extra‐mammary Paget's disease

Malassezia‐derived aryl hydrocarbon receptor ligands enhance the CCL20/Th17/soluble CD163 pathogenic axis in extra‐mammary Paget's disease

An adolescent girl with atrophic plaques on her trunk

Host Responses to Malassezia spp. in the Mammalian Skin

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