Blood endotyping distinguishes the profile of vitiligo from that of other inflammatory and autoimmune skin diseases

Czarnowicki, Tali; He, Helen; Leonard, Alexandra; Kim, Hyun Je; Kameyama, Naoya; Pavel, Ana B.; Li, Randall; Estrada, Yeriel; Wen, Huei‐Chi; Kimmel, Grace W.; Kim, Hee J.; Chima, Margot; Lebwohl, Mark; Krueger, James G.; Guttman‐Yassky, Emma

doi:10.1016/j.jaci.2018.11.031

Cited by 48 publications

(50 citation statements)

References 93 publications

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“…Unsupervised hierarchical clustering of all T-cell subset frequencies, clinical scores, AD duration, and age was performed by using Spearman correlations as a similarity metric, as displayed in the correlation heat map and dendrogram in Fig 5 (red, positive correlation; blue, negative correlation; stars and plus signs display significance). Congruent with recent AD data, 22,26 which showed positive correlations between IL-13-and IL-22-producing and IL-17-and IL-22-producing T cells, 22,26,27 these cytokines largely grouped together. IFN-g-producing T-cells clustered together with AD duration and patient age.…”

Section: T-cell Activation Clinical Measures and Ifn-g Levels Are Asupporting

confidence: 50%

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Evolution of pathologic T-cell subsets in patients with atopic dermatitis from infancy to adulthood

Czarnowicki

Canter

et al. 2020

Journal of Allergy and Clinical Immunology

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Section: T-cell Activation Clinical Measures and Ifn-g Levels Are Asupporting

confidence: 50%

“…73 Studies have shown positive correlations and cellular coproduction of IL-13 and IL-22 22,74 and of IL-17 and IL-22. 27,75 Indeed, these markers cluster together in the correlation heat map. IFN-g clusters with patient age and disease duration, differentiating infants from children and adolescents and adolescents from adults with AD.…”

Section: Discussionmentioning

confidence: 96%

Evolution of pathologic T-cell subsets in patients with atopic dermatitis from infancy to adulthood

Czarnowicki

Canter

et al. 2020

Journal of Allergy and Clinical Immunology

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“…The effector CD4 1 T-cell response also participates in vitiligo development. 31,32 We found that CD4 1 T cells from both patients with vitiligo and healthy control subjects expressed IL-1R (Fig 7, D) and that H 2 O 2 -treated HaCaT supernatants promoted secretion of IFN-g, IL-17A, and IL-17F in CD4 1 T cells from patients with vitiligo, which were abolished by TRPM2 or NLRP3 knockdown in HaCaT cells or by IL-1b/ IL-1R signaling blocking in the incubation system (Fig 7, E-G). However, in CD4 1 T cells from healthy control subjects,…”

Section: Trpm2-mediated Nlrp3 Inflammasome Activation In Keratinocytementioning

confidence: 99%

Activated NLR family pyrin domain containing 3 (NLRP3) inflammasome in keratinocytes promotes cutaneous T-cell response in patients with vitiligo

Kang

Zhang

et al. 2020

Journal of Allergy and Clinical Immunology

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Background: Keratinocytes can function as innate immune cells under oxidative stress and aggravate the cutaneous T-cell response that undermines melanocytes in the setting of vitiligo. The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is a regulator of innate immunity that exists in keratinocytes. However, the role of the NLRP3 inflammasome in the pathogenesis of vitiligo has not been investigated. Objective: We sought to explicate the contribution of the activated NLRP3 inflammasome in keratinocytes to the autoimmune response in patients with vitiligo.Methods: Perilesional and serum samples from patients with vitiligo were collected to examine the status of the NLRP3 inflammasome in the setting of vitiligo. Cultured keratinocytes were treated with H 2 O 2 to investigate the mechanism for NLRP3 inflammasome activation under oxidative stress. Peripheral blood T cells were extracted from patients with vitiligo to explore the influence of the NLRP3 inflammasome on the T-cell response in patients with vitiligo. Results: Expressions of NLRP3 and downstream cytokine IL-1b were consistently increased in perilesional keratinocytes of patients with vitiligo. Notably, serum IL-1b levels were From a

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“…78 Treg cells are essential regulators of the immune system, and their alteration in number and function has been implicated in several inflammatory diseases. [79][80][81][82][83][84] Therefore a defect in Treg cell function has piqued the interest of investigators in the context of AA pathogenesis. 12,[85][86][87][88][89] Given that the eye is one of the major immune-privileged sites of mammals, key pointers arise from ophthalmologic research, and HF IP research might also inform human eye IP research.…”

Section: Is Aa a Model Disease For An Imbalance Between Cytotoxic Effmentioning

confidence: 99%

Frontiers in alopecia areata pathobiology research

Gilhar

Laufer-Britva

Keren

et al. 2019

Journal of Allergy and Clinical Immunology

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This current review explores selected and as yet insufficiently investigated frontiers in current alopecia areata (AA) pathobiology research, with an emphasis on potential ''new'' players in AA pathobiology that deserve more systematic exploration and therapeutic targeting. Indeed, new evidence suggests that CD8 1 T cells, which have long been thought to be the central players in AA pathobiology, are not the only drivers of disease. Instead, subsets of natural killer (NK) and so-called ''unconventional'' T cells (invariant NK T cells, gd T cells, classic NK cells, and type 1 innate lymphoid cells), all of which can produce large amounts of IFN-g, might also drive AA pathobiology independent of classical, autoantigen-dependent CD8 1 T-cell functions. Another important new frontier is the role of regulatory lymphocyte subsets, such as regulatory T cells, gd regulatory T cells, NKT10 cells, and perifollicular mast cells, in maintaining physiologic hair follicle immune privilege (IP); the extent to which these functions are defective in patients with AA; and how this IP-protective role could be restored therapeutically in patients with established AA. Broadening our AA research horizon along the lines suggested above promises not only to open the door to innovative and even more effective immunotherapy strategies for AA but will also likely be relevant for other autoimmune disorders in which pathobiology, ectopic MHC class I expression, and IP collapse play an important role.

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Blood endotyping distinguishes the profile of vitiligo from that of other inflammatory and autoimmune skin diseases

Abstract: Multicytokine polarization in blood distinguishes vitiligo from other inflammatory skin diseasesTh1/Tc1 N PSO AD AA Vitiligo

Cited by 48 publications

References 93 publications

Evolution of pathologic T-cell subsets in patients with atopic dermatitis from infancy to adulthood

Evolution of pathologic T-cell subsets in patients with atopic dermatitis from infancy to adulthood

Activated NLR family pyrin domain containing 3 (NLRP3) inflammasome in keratinocytes promotes cutaneous T-cell response in patients with vitiligo

Frontiers in alopecia areata pathobiology research

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