Missing Insight Into T and B Cell Responses in Dermatitis Herpetiformis

Dermatitis herpetiformis is a cutaneous form of celiac disease manifesting as an itching rash typically on the elbows, knees and buttocks. It is driven by the ingestion of gluten-containing cereals and characterized by granular deposits of immunoglobulin A in the papillary dermis. These antibodies t...

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Main Authors: Esko Kemppainen, Teea Salmi, Katri Lindfors
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-03-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2021.657280/full
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author Esko Kemppainen
Teea Salmi
Teea Salmi
Katri Lindfors
author_facet Esko Kemppainen
Teea Salmi
Teea Salmi
Katri Lindfors
author_sort Esko Kemppainen
collection DOAJ
description Dermatitis herpetiformis is a cutaneous form of celiac disease manifesting as an itching rash typically on the elbows, knees and buttocks. It is driven by the ingestion of gluten-containing cereals and characterized by granular deposits of immunoglobulin A in the papillary dermis. These antibodies target transglutaminase (TG) 3 and in the majority of patients they are also found in circulation. The circulating antibodies disappear and skin symptoms resolve as a result of gluten-free diet but the cutaneous anti-TG3 IgA deposits may persist for several years. In dermatitis herpetiformis, plasma cells secreting antibodies against TG3 are located in the intestinal mucosa similarly to those producing TG2 antibodies characteristic for celiac disease. In fact, both TG2- and TG3-specific plasma cells and gluten responsive T cells are found in dermatitis herpetiformis patients but the interplay between these cell populations is unknown. The small bowel mucosal damage in celiac disease is believed to be mediated by co-operation of cytotoxic intraepithelial T cells and the inflammatory milieu contributed by gluten-reactive CD4+ T cells, whereas the skin lesions in dermatitis herpetiformis appear to be devoid of gluten reactive T cells. Thus, how celiac disease-type intestinal T and B cell responses develop into an autoimmune condition affecting the skin is still incompletely understood. Finally, the skin and small bowel lesions may reappear upon reintroduction of gluten in patients treated with gluten-free diet but virtually nothing is known about the long-lived B cell and memory T cell populations activating in response to dietary gluten in dermatitis herpetiformis.
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spelling doaj.art-54c72171531d4cdb8bfaa47d3d0a96462022-12-21T21:26:21ZengFrontiers Media S.A.Frontiers in Immunology1664-32242021-03-011210.3389/fimmu.2021.657280657280Missing Insight Into T and B Cell Responses in Dermatitis HerpetiformisEsko Kemppainen0Teea Salmi1Teea Salmi2Katri Lindfors3Celiac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, FinlandCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, FinlandDepartment of Dermatology, Tampere University Hospital, Tampere, FinlandCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, FinlandDermatitis herpetiformis is a cutaneous form of celiac disease manifesting as an itching rash typically on the elbows, knees and buttocks. It is driven by the ingestion of gluten-containing cereals and characterized by granular deposits of immunoglobulin A in the papillary dermis. These antibodies target transglutaminase (TG) 3 and in the majority of patients they are also found in circulation. The circulating antibodies disappear and skin symptoms resolve as a result of gluten-free diet but the cutaneous anti-TG3 IgA deposits may persist for several years. In dermatitis herpetiformis, plasma cells secreting antibodies against TG3 are located in the intestinal mucosa similarly to those producing TG2 antibodies characteristic for celiac disease. In fact, both TG2- and TG3-specific plasma cells and gluten responsive T cells are found in dermatitis herpetiformis patients but the interplay between these cell populations is unknown. The small bowel mucosal damage in celiac disease is believed to be mediated by co-operation of cytotoxic intraepithelial T cells and the inflammatory milieu contributed by gluten-reactive CD4+ T cells, whereas the skin lesions in dermatitis herpetiformis appear to be devoid of gluten reactive T cells. Thus, how celiac disease-type intestinal T and B cell responses develop into an autoimmune condition affecting the skin is still incompletely understood. Finally, the skin and small bowel lesions may reappear upon reintroduction of gluten in patients treated with gluten-free diet but virtually nothing is known about the long-lived B cell and memory T cell populations activating in response to dietary gluten in dermatitis herpetiformis.https://www.frontiersin.org/articles/10.3389/fimmu.2021.657280/fulldermatitis herpetiformisceliac diseaseT cellB cellepitope spreadingtransglutaminase
spellingShingle Esko Kemppainen
Teea Salmi
Teea Salmi
Katri Lindfors
Missing Insight Into T and B Cell Responses in Dermatitis Herpetiformis
Frontiers in Immunology
dermatitis herpetiformis
celiac disease
T cell
B cell
epitope spreading
transglutaminase
title Missing Insight Into T and B Cell Responses in Dermatitis Herpetiformis
title_full Missing Insight Into T and B Cell Responses in Dermatitis Herpetiformis
title_fullStr Missing Insight Into T and B Cell Responses in Dermatitis Herpetiformis
title_full_unstemmed Missing Insight Into T and B Cell Responses in Dermatitis Herpetiformis
title_short Missing Insight Into T and B Cell Responses in Dermatitis Herpetiformis
title_sort missing insight into t and b cell responses in dermatitis herpetiformis
topic dermatitis herpetiformis
celiac disease
T cell
B cell
epitope spreading
transglutaminase
url https://www.frontiersin.org/articles/10.3389/fimmu.2021.657280/full
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