T cell participation in autoreactivity to NC16a epitopes in bullous pemphigoid

Pickford, Wendy; Gudi, V.; Haggart, A. M.; Lewis, B. J.; Herriot, Richard; Barker, Robert N.; Ormerod, Anthony

doi:10.1111/cei.12566

Cited by 22 publications

(26 citation statements)

References 53 publications

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“…Both CCL17 and CCL22 are ligands of CCR4, suggesting the recruitment of Th2 and regulatory T cells in lesional skin . Since Th2 contributes to the pathogenesis of BP, we hypothesized that CCL17 and CCL22 produced by CD163 M2 macrophages increase serum CCL17 and CCL22 levels in BP patients. In our present study, serum CCL22 was increased in BP patients compared with healthy donors, and CD163 + M2 macrophages produced CCL22 in the lesional skin of BP.…”

Section: Discussionmentioning

confidence: 99%

Minocycline decreases Th2 chemokines from M2 macrophages: Possible mechanisms for the suppression of bullous pemphigoid by traditional bullous disease drugs

Tanita

Fujimura

Sato

et al. 2018

Experimental Dermatology

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Minocycline/tetracycline is clinically used for the treatment of bullous pemphigoid (BP), and its clinical benefits are superior to those of prednisolone when considering adverse events. Although the clinical benefits of minocycline/tetracycline are well known, its immunosuppressive mechanisms are still unclear. In this study, we investigated the immunomodulatory effects of traditional anti-BP drugs (minocycline, nicotinic acid amide, dexamethasone and cyclosporine) on CD163 M2 macrophages in vitro, with special focus on the production of CCL18 and CCL22, both of which are produced by CD163 M2 macrophages in the lesional skin of BP and are increased in the serum of BP patients. Minocycline decreased the production of CCL22, CCL24 and CCL26 as well as CCL2 from M2 macrophages. CCL18 from M2 macrophages was decreased by dexamethasone and cyclosporine, but not decreased by minocycline. These data suggest that the clinical benefit of minocycline is partially explained by its suppressive effects against the production of specific Th2 chemokines from M2 macrophages, which should contribute to the recruitment of Th2 cells and eosinophils in the lesional skin of BP patients.

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Section: Discussionmentioning

confidence: 99%

Minocycline decreases Th2 chemokines from M2 macrophages: Possible mechanisms for the suppression of bullous pemphigoid by traditional bullous disease drugs

Tanita

Fujimura

Sato

et al. 2018

Experimental Dermatology

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“…[108] In this context, the specific T cell response after challenge with NC16A, as measured by the release of IL-4 and IgE response, was significantly stronger in BP patients compared to controls, pointing to an important contribution by Th2 cytokines to pathogenesis. [109] Interestingly, two reports related BP to sensitization with specific allergens, hen's egg allergen and penicillins, as demonstrated by specific serum IgE, patch testing, and basophil histamine release test. [103,110] …”

Section: Bp180-specific Ige Autoantibodiesmentioning

confidence: 99%

IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

Beek

Schulze

Zillikens

et al. 2015

Expert Review of Clinical Immunology

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Autoimmune bullous diseases (AIBDs) are characterized by autoantibodies against structural proteins of the dermal-epidermal junction (in pemphigoid diseases) and the epidermal/ epithelial desmosomes (in pemphigus diseases). By far, the most common AIBD is bullous pemphigoid, which is immunopathologically characterized by autoantibodies against BP180 (type XVII collagen) and BP230. IgG and, to a lesser extent, IgA autoantibodies are the major autoantibody isotypes in these disorders. IgE autoantibodies are increasingly reported in particular in bullous pemphigoid. The development of specific and sensitive anti-BP180 IgE ELISA systems, the report of two experimental murine models employing IgE autoantibodies against BP180, and the successful treatment of bullous pemphigoid with the anti-IgE antibody omalizumab have raised interest in the role of IgE autoantibodies and the modulation of their production in AIBDs. Here, the relevance of IgE autoantibodies in the diagnosis, pathophysiology, and treatment decisions of AIBDs, with a focus on bullous pemphigoid, is reviewed. ARTICLE HISTORY

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“…Previous work has shown that peripheral blood T cells from patients with BP proliferate with exposure to specific BP180 antigenic epitopes and secrete cytokines consistent with a combined Th1 and Th2 phenotype . Pickford et al found that BP180 antigen exposure to peripheral blood T cells resulted in a Th2 pattern of response . In lesional skin of BP, two studies showed a reduction in the number of T‐regulatory cells compared to other inflammatory dermatoses such as psoriasis, atopic dermatitis and pemphigus vulgaris.…”

Section: Discussionmentioning

confidence: 99%

Cutaneous autoimmune effects in the setting of therapeutic immune checkpoint inhibition for metastatic melanoma

et al. 2016

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Therapeutic immune checkpoint blockade for metastatic melanoma has been associated with vitiligo, pruritus and morbilliform eruptions. Reports of other autoimmune skin disease in this setting are rare. We sought to expand the spectrum of cutaneous immune-mediated effects related to immune checkpoint inhibitor therapy. In this report, we describe two unusual cutaneous reactions related to checkpoint inhibitor therapy, namely bullous pemphigoid (BP) and dermatitis herpetiformis. The development of BP and dermatitis herpetiformis in the context of checkpoint inhibitor therapy is consistent with previous investigations supporting the importance of effector and regulatory T cells in the pathogenesis of these diseases.

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T cell participation in autoreactivity to NC16a epitopes in bullous pemphigoid

Abstract: SummaryBullous pemphigoid is a blistering skin disease characterized by autoantibodies against the NC16a domain of bullous pemphigoid 180. This study was performed to characterize and map the fine specificity of T cell responses to NC16a.

Cited by 22 publications

References 53 publications

Minocycline decreases Th2 chemokines from M2 macrophages: Possible mechanisms for the suppression of bullous pemphigoid by traditional bullous disease drugs

Minocycline decreases Th2 chemokines from M2 macrophages: Possible mechanisms for the suppression of bullous pemphigoid by traditional bullous disease drugs

IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

Cutaneous autoimmune effects in the setting of therapeutic immune checkpoint inhibition for metastatic melanoma

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