Psoriasis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
There are two main hypotheses about the process that occurs in the development of the disease. The first considers psoriasis as primarily a disorder of excessive growth and reproduction of skin cells. The problem is simply seen as a fault of the [[epidermis (skin)|epidermis]] and its [[keratinocytes]]. The second hypothesis sees the disease as being an [[immune-mediated disease|immune-mediated disorder]] in which the excessive reproduction of skin cells is secondary to factors produced by the [[immune system]]. [[T cell]]s (which normally help protect the body against infection) become active, migrate to the [[dermis]] and trigger the release of [[cytokines]] ([[tumor necrosis factor-alpha]] TNFα, in particular) which cause inflammation and the rapid production of skin cells. It is not known what initiates the activation of the T cells. | |||
The immune-mediated model of psoriasis has been supported by the observation that [[immunosuppressant]] medications can clear psoriasis plaques. However, the role of the immune system is not fully understood, and it has recently been reported that an [[animal model]] of psoriasis can be triggered in mice lacking T cells.<!-- | |||
--><ref name=Zenz>{{cite journal |author=Zenz R, Eferl R, Kenner L, ''et al'' |title=Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins |journal=Nature |volume=437 |issue=7057 |pages=369–75 |year=2005 |pmid=16163348 |doi=10.1038/nature03963}}</ref> [[Animal model]]s, however, reveal only a few aspects resembling human psoriasis. | |||
===Genetics=== | ===Genetics=== | ||
Revision as of 17:59, 22 August 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
There are two main hypotheses about the process that occurs in the development of the disease. The first considers psoriasis as primarily a disorder of excessive growth and reproduction of skin cells. The problem is simply seen as a fault of the epidermis and its keratinocytes. The second hypothesis sees the disease as being an immune-mediated disorder in which the excessive reproduction of skin cells is secondary to factors produced by the immune system. T cells (which normally help protect the body against infection) become active, migrate to the dermis and trigger the release of cytokines (tumor necrosis factor-alpha TNFα, in particular) which cause inflammation and the rapid production of skin cells. It is not known what initiates the activation of the T cells.
The immune-mediated model of psoriasis has been supported by the observation that immunosuppressant medications can clear psoriasis plaques. However, the role of the immune system is not fully understood, and it has recently been reported that an animal model of psoriasis can be triggered in mice lacking T cells.[1] Animal models, however, reveal only a few aspects resembling human psoriasis.
Genetics
Around one-third of people with psoriasis report a family history of the disease, and researchers have identified genetic loci associated with the condition. Studies of monozygotic twins suggest a 70% chance of a twin developing psoriasis if the other twin has psoriasis. The concordance is around 20% for dizygotic twins. These findings suggest both a genetic predisposition and an environmental response in developing psoriasis.[2]
References
- ↑ Zenz R, Eferl R, Kenner L; et al. (2005). "Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins". Nature. 437 (7057): 369–75. doi:10.1038/nature03963. PMID 16163348.
- ↑ Krueger G, Ellis CN (2005). "Psoriasis--recent advances in understanding its pathogenesis and treatment". J. Am. Acad. Dermatol. 53 (1 Suppl 1): S94–100. doi:10.1016/j.jaad.2005.04.035. PMID 15968269.