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,...
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Dove Medical Press
2016
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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) |
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Psoriasis Inflammation Autoimmune disease Comorbidity Dermatology RL1-803 |
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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 |
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