Current knowledge on psoriasis and autoimmune diseases

Nilmarie Ayala-Fontánez,1,2 David C Soler,1,2 Thomas S McCormick1,2 1Department of Dermatology, Case Western Reserve University, Cleveland, OH, USA; 2The Murdough Family Center for Psoriasis, University Hospitals Case Medical Center, Cleveland, OH, USA Abstract: Psoriasis is a prevalent,...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Ayala-Fontánez N, Soler DC, McCormick TS
Formato: article
Lenguaje:EN
Publicado: Dove Medical Press 2016
Materias:
Acceso en línea:https://doaj.org/article/adf4d6292d4e442a84783b2e0e213313
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:adf4d6292d4e442a84783b2e0e213313
record_format dspace
spelling oai:doaj.org-article:adf4d6292d4e442a84783b2e0e2133132021-12-02T05:10:16ZCurrent knowledge on psoriasis and autoimmune diseases2230-326Xhttps://doaj.org/article/adf4d6292d4e442a84783b2e0e2133132016-02-01T00:00:00Zhttps://www.dovepress.com/current-knowledge-on-psoriasis-and-autoimmune-diseases-peer-reviewed-article-PTThttps://doaj.org/toc/2230-326XNilmarie Ayala-Fontánez,1,2 David C Soler,1,2 Thomas S McCormick1,2 1Department of Dermatology, Case Western Reserve University, Cleveland, OH, USA; 2The Murdough Family Center for Psoriasis, University Hospitals Case Medical Center, Cleveland, OH, USA Abstract: Psoriasis is a prevalent, chronic inflammatory disease of the skin, mediated by crosstalk between epidermal keratinocytes, dermal vascular cells, and immunocytes such as antigen presenting cells (APCs) and T cells. Exclusive cellular “responsibility” for the induction and maintenance of psoriatic plaques has not been clearly defined. Increased proliferation of keratinocytes and endothelial cells in conjunction with APC/T cell/monocyte/macrophage inflammation leads to the distinct epidermal and vascular hyperplasia that is characteristic of lesional psoriatic skin. Despite the identification of numerous susceptibility loci, no single genetic determinant has been identified as responsible for the induction of psoriasis. Thus, numerous other triggers of disease, such as environmental, microbial and complex cellular interactions must also be considered as participants in the development of this multifactorial disease. Recent advances in therapeutics, especially systemic so-called “biologics” have provided new hope for identifying the critical cellular targets that drive psoriasis pathogenesis. Recent recognition of the numerous co-morbidities and other autoimmune disorders associated with psoriasis, including inflammatory bowel disease, multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus suggest common signaling elements and cellular mediators may direct disease pathogenesis. In this review, we discuss common cellular pathways and participants that mediate psoriasis and other autoimmune disorders that share these cellular signaling pathways. Keywords: psoriasis, autoimmunity, immunosuppressionAyala-Fontánez NSoler DCMcCormick TSDove Medical PressarticlePsoriasisInflammationAutoimmune diseaseComorbidityDermatologyRL1-803ENPsoriasis: Targets and Therapy, Vol 2016, Iss Issue 1, Pp 7-32 (2016)
institution DOAJ
collection DOAJ
language EN
topic Psoriasis
Inflammation
Autoimmune disease
Comorbidity
Dermatology
RL1-803
spellingShingle Psoriasis
Inflammation
Autoimmune disease
Comorbidity
Dermatology
RL1-803
Ayala-Fontánez N
Soler DC
McCormick TS
Current knowledge on psoriasis and autoimmune diseases
description Nilmarie Ayala-Fontánez,1,2 David C Soler,1,2 Thomas S McCormick1,2 1Department of Dermatology, Case Western Reserve University, Cleveland, OH, USA; 2The Murdough Family Center for Psoriasis, University Hospitals Case Medical Center, Cleveland, OH, USA Abstract: Psoriasis is a prevalent, chronic inflammatory disease of the skin, mediated by crosstalk between epidermal keratinocytes, dermal vascular cells, and immunocytes such as antigen presenting cells (APCs) and T cells. Exclusive cellular “responsibility” for the induction and maintenance of psoriatic plaques has not been clearly defined. Increased proliferation of keratinocytes and endothelial cells in conjunction with APC/T cell/monocyte/macrophage inflammation leads to the distinct epidermal and vascular hyperplasia that is characteristic of lesional psoriatic skin. Despite the identification of numerous susceptibility loci, no single genetic determinant has been identified as responsible for the induction of psoriasis. Thus, numerous other triggers of disease, such as environmental, microbial and complex cellular interactions must also be considered as participants in the development of this multifactorial disease. Recent advances in therapeutics, especially systemic so-called “biologics” have provided new hope for identifying the critical cellular targets that drive psoriasis pathogenesis. Recent recognition of the numerous co-morbidities and other autoimmune disorders associated with psoriasis, including inflammatory bowel disease, multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus suggest common signaling elements and cellular mediators may direct disease pathogenesis. In this review, we discuss common cellular pathways and participants that mediate psoriasis and other autoimmune disorders that share these cellular signaling pathways. Keywords: psoriasis, autoimmunity, immunosuppression
format article
author Ayala-Fontánez N
Soler DC
McCormick TS
author_facet Ayala-Fontánez N
Soler DC
McCormick TS
author_sort Ayala-Fontánez N
title Current knowledge on psoriasis and autoimmune diseases
title_short Current knowledge on psoriasis and autoimmune diseases
title_full Current knowledge on psoriasis and autoimmune diseases
title_fullStr Current knowledge on psoriasis and autoimmune diseases
title_full_unstemmed Current knowledge on psoriasis and autoimmune diseases
title_sort current knowledge on psoriasis and autoimmune diseases
publisher Dove Medical Press
publishDate 2016
url https://doaj.org/article/adf4d6292d4e442a84783b2e0e213313
work_keys_str_mv AT ayalafontanezn currentknowledgeonpsoriasisandautoimmunediseases
AT solerdc currentknowledgeonpsoriasisandautoimmunediseases
AT mccormickts currentknowledgeonpsoriasisandautoimmunediseases
_version_ 1718400553099198464