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| ==Causes== | | ==Causes== |
| ===Common Causes===
| | Psoriasis is caused due to the presence of various genetic, environmental and behavioral risk factors in an individual. The presence of these risk factors may cause an activation of the immune system which may lead to disease. The factors which may increase the susceptibility to developing psoriasis can be found at |
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| ==== Genetics<ref name="pmid16916825">{{cite journal |vauthors=Smith CH, Barker JN |title=Psoriasis and its management |journal=BMJ |volume=333 |issue=7564 |pages=380–4 |year=2006 |pmid=16916825 |pmc=1550454 |doi=10.1136/bmj.333.7564.380 |url=}}</ref> ====
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| * The human genome has at least nine different loci , which lead to the development of psoriasis (PSORS1-9).
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| * PSORS-1, a part of the major histocompatibility complex (MHC) on chromosome 6p2, is the major genetic determinant of psoriasis, and is responsible for up to fifty percent of genetic susceptibility to the disease.<ref name="pmid16138103">{{cite journal |vauthors=Bowcock AM, Krueger JG |title=Getting under the skin: the immunogenetics of psoriasis |journal=Nat. Rev. Immunol. |volume=5 |issue=9 |pages=699–711 |year=2005 |pmid=16138103 |doi=10.1038/nri1689 |url=}}</ref>
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| * The second most well-characterized disease-susceptibility locus (''PSORS2'') is found within 17q24–q25.
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| * Misssense mutations in CARD14 gene lead to activation of the NF-κB pathway.
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| * Another major gene involved in the development of psoriasis is a HLA class I allele, specifically HLA-Cw6.<ref name="pmid7387872">{{cite journal |vauthors=Tiilikainen A, Lassus A, Karvonen J, Vartiainen P, Julin M |title=Psoriasis and HLA-Cw6 |journal=Br. J. Dermatol. |volume=102 |issue=2 |pages=179–84 |year=1980 |pmid=7387872 |doi= |url=}}</ref>
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| ==== Immune system ====
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| * Both innate and adaptive immunity is involved in the development of psoriasis.
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| * The key cytokines of immune system, which lead to psoriasis are tumor necrosis factor-alpha and interferon alpha.
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| * The LFA-1 integrin is also important in the immune pathogenesis of psoriasis and has been known to be a target for medications used for the management of psoriasis.
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| * Within the immune system, development of psoriasis is based upon four key pathways/interactions:
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| ** Antigen presentation
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| ** NF-κB signaling
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| ** IL-23/IL-17 axis
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| ** Type I IFN pathway.
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| ==== Environmental and behavioral ====
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| The enviromental factors implicated in the development or aggravation of psoriasis are:<ref>[http://www.skincarephysicians.com/psoriasisnet/triggers.html <nowiki>[1]</nowiki>] Psoriasis Triggers at Psoriasis Net. SkinCarePhysicians.com 9-28-05. American Academy of Dermatology, 2008.</ref><ref>{{cite journal |author=Behnam SM, Behnam SE, Koo JY |title=Smoking and psoriasis |journal=Skinmed |volume=4 |issue=3 |pages=174–6 |year=2005 |pmid=15891254 |doi= |url=http://www.lejacq.com/articleDetail.cfm?pid=SKINmed_4;3:174}}</ref><ref>[http://www.medscape.com/viewarticle/556533 <nowiki>[2]</nowiki>][http://dermatology.cdlib.org/132/reviews/HIV/fife.html <nowiki>[3]</nowiki>] Fife, Jeffes, Koo, Waller. Unraveling the Paradoxes of HIV-associated Psoriasis: A Review of T-cell Subsets and Cytokine Profiles. 5-18-07. Retrieved 5-13-08.</ref><ref>{{cite journal |author=Ortonne JP, Lebwohl M, Em Griffiths C |title=Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis |journal=Eur J Dermatol |volume=13 |issue=2 |pages=117–23 |year=2003 |pmid=12695125 |doi= |url=http://www.john-libbey-eurotext.fr/medline.md?issn=1167-1122&vol=13&iss=2&page=117}}</ref><ref>{{cite journal |author=Austin LM, Ozawa M, Kikuchi T, Walters IB, Krueger JG |title=The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients |journal=J. Invest. Dermatol. |volume=113 |issue=5 |pages=752–9 |year=1999 |month=November |pmid=10571730 |doi=10.1046/j.1523-1747.1999.00749.x |url=}}</ref><ref>[http://www.nsc.gov.sg/cgi-bin/WB_ContentGen.pl?id=401&gid=83 <nowiki>[4]</nowiki>] A Case Report of Severe Psoriasis in a Patient with AIDS: The Role of the HIV Virus and the Therapeutic Challenges Involved. Vol: 13 No 2, 2002. National Skin Center. Retrieved 05-13-08.</ref><ref name="pmid15199399">{{cite journal |vauthors=Nickoloff BJ, Nestle FO |title=Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities |journal=J. Clin. Invest. |volume=113 |issue=12 |pages=1664–75 |year=2004 |pmid=15199399 |pmc=420513 |doi=10.1172/JCI22147 |url=}}</ref>
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| **Stress (physical and mental)
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| **Smoking
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| **Excessive alcohol consumption
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| **Infection (Streptococcal, HIV
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| **Seasonal variation
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| **Medications (Lithium, Beta blockers, pegylated interferon alpha-2b, Siltuximab)
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| **Obesity
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| **Skin injury
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| **Skin dryness
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| ==References== | | ==References== |