Clinical perspectives and murine models of lichenoid tissue reaction/interface dermatitis

Okiyama, Naoko; Fujimoto, Manabu

doi:10.1016/j.jdermsci.2015.03.001

Cited by 22 publications

(21 citation statements)

References 52 publications

(61 reference statements)

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“…37 This reaction pattern may be due to the nonspecific activation of T-cells (as a result of PD-1 receptor blockade), which may be targeting antigen (drug)-presenting keratinocytes in susceptible individuals. 38 An instance of psoriasiform eruption has also been documented. 39 In our patients, mostly medium-to-high potency topical (and sometimes oral) corticosteroids sufficed for the treatment of rashes due to either drug, although this could vary depending upon the clinical severity.…”

Section: Discussionmentioning

confidence: 99%

Characterisation and management of dermatologic adverse events to agents targeting the PD-1 receptor

Belum

Benhuri

Postow

et al. 2016

European Journal of Cancer

340

343

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CONFLICT OF INTEREST STATEMENT VRB, BB, MDH, NHS, RJM, and KJB have no conflicts of interest to declare. MAP has had a consulting or advisory role with Amgen and Bristol-Myers Squibb, and receives research support from Bristol-Myers Squibb and Novartis (Inst). AML has a consulting or advisory role with Bristol-Myers Squibb, Janssen, Aduro, Efranat, Jounce, and Novartis, and receives research funding from Bristol-Myers Squibb (Inst), Janssen (Inst.), and Genentech (Inst). SW has a speaking arrangement with Novartis, Bayer-Onyx, Pfizer, and Mediavation. JDW has a consulting or advisory role with Bristol-Myers Squibb, Merck, MedImmune, Ziopharm, Polynoma, Polaris, Jounce, GlaxoSmithKline; receives honoraria from EMD Serono, Janssen Oncology, and research funding from Bristol-Myers Squibb (Inst), MedImmune (Inst), GlaxoSmithKline (Inst), Merck (Inst). MEL has consulted for BMS and Merck, and received research support from Bristol-Myers Squibb (Inst).Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. HHS Public Access AbstractBackground-Dermatologic adverse events (AEs) are some of the most frequently observed toxicities of immune-checkpoint inhibitor therapy, but have received little attention. The drugs, pembrolizumab and nivolumab are recently approved inhibitors of the PD-1 receptor that have overlapping AE profiles however, the incidence, relative risk (RR), and clinico-morphological pattern of the associated dermatologic AEs is not known.

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Section: Discussionmentioning

confidence: 99%

Characterisation and management of dermatologic adverse events to agents targeting the PD-1 receptor

Belum

Benhuri

Postow

et al. 2016

European Journal of Cancer

340

343

View full text Add to dashboard Cite

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“…In line with that observation, transcriptional network comparison of lesional lichen planus and lupus erythematosus with non‐interface skin diseases revealed that differentially expressed genes are attributable to type 1 lymphocytes as well as to the effect of IFN‐γ on keratinocytes, including apoptosis and necroptosis (unpublished data). Furthermore, interface dermatitis is induced in murine models of xenotransplantation or adoptive transfer of keratinocyte‐reactive cytotoxic T cells . In cell culture models, FasL induces the characteristic hypergranulosis while IFN‐γ causes keratinocyte apoptosis with cytoid body formation, and ICAM‐1 expression .…”

Section: An Immunologic View At Inflammatory Skin Diseasesmentioning

confidence: 99%

“…Furthermore, interface dermatitis is induced in murine models of xenotransplantation or adoptive transfer of keratinocyte-reactive cytotoxic T cells. 7 In cell culture models, FasL induces the characteristic hypergranulosis while IFN-c causes keratinocyte apoptosis with cytoid body formation, and ICAM-1 expression. 8 Increasing evidence suggests an additional and important role for plasmacytoid dendritic cells and IFN-a in the pathogenesis of lichenoid diseases, possibly via recruitment and amplification of interface dermatitis.…”

Section: Lichenoid Pattern (Pattern 1)mentioning

confidence: 99%

Immune response patterns in non‐communicable inflammatory skin diseases

Eyerich

2018

Acad Dermatol Venereol

116

143

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Non‐communicable inflammatory skin diseases (ncISD) such as psoriasis or atopic eczema are a major cause of global disease burden. Due to their impact and complexity, ncISD represent a major challenge of modern medicine. Dermatology textbooks describe more than 100 different ncISD based on clinical phenotype and histological architecture. In the last decades, this historical description was complemented by increasing molecular knowledge – and this knowledge is now being translated into specific therapeutics. Combining the enormous advances made in lymphocyte immunology and molecular genetics with clinical and histological phenotyping reveals six immune response patterns of the skin – type I immune cells cause the lichenoid pattern characterized by immune‐mediated cell death of keratinocytes; type II immune cells underlie the eczematous pattern with impaired epidermal barrier, infection and eosinophils as well as the bullous pattern with loss of epithelial integrity; Th17 cells and ILC3 mediate the psoriatic pattern characterized by acanthosis, high metabolic activity and neutrophils; dysbalance of regulatory T cells causes either the fibrogenic pattern with rarefication of cells and dermal thickening or the granulomatous pattern defined by formation of granulomas. With more and more specific therapeutic agents approved, classifying ncISD also according to their immune response pattern will become highly relevant. This review defines the six immune response patterns of ncISD and highlights therapeutic strategies targeting key lymphocyte mediators.

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“…This phenomenon may be explained by evidence pointing to keratinocytes as the central target in lichenoid tissue reactions, leading to increased keratinocyte necrosis compared with melanoma. 14,16 In addition, nearly half of regressed melanoma specimens showed a dense band of melanophages in the papillary dermis. This feature was not observed in any of the regressed LPLK, all of which exhibited a pattern of sparse perivascular melanophages.…”

Section: Resultsmentioning

confidence: 99%