Psoriasis risk factors

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]


Common risk factors in the development of psoriasis are genes which increase the susceptibility of developing psoriasis and environmental triggers. The presence of these risk factors may lead to auto-immunity and development of psoriasis.

Risk Factors

Common Risk Factors


  • The human genome has at least nine different loci implicated in the development of psoriasis (PSORS1-9).[1]
  • 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 50% of genetic susceptibility to the disease.[2]
  • The second most well-characterized disease-susceptibility locus (PSORS2) is found within 17q24–q25.
  • Missense mutations in CARD14 gene lead to activation of the NF-κB pathway.
  • Another major gene involved in the development of psoriasis is a HLA class I allele, specifically HLA-Cw6.[3]
  • Psoriatic arthritis (PsA) has been shown to be associated with human leukocyte antigen (HLA) class 1.[4]

Immune system

Environmental and behavioral

The environmental factors implicated in the development or aggravation of psoriasis are:[5][6][7][8][9][10][11]


  1. Smith CH, Barker JN (2006). "Psoriasis and its management". BMJ. 333 (7564): 380–4. doi:10.1136/bmj.333.7564.380. PMC 1550454. PMID 16916825.
  2. Bowcock AM, Krueger JG (2005). "Getting under the skin: the immunogenetics of psoriasis". Nat. Rev. Immunol. 5 (9): 699–711. doi:10.1038/nri1689. PMID 16138103.
  3. Tiilikainen A, Lassus A, Karvonen J, Vartiainen P, Julin M (1980). "Psoriasis and HLA-Cw6". Br. J. Dermatol. 102 (2): 179–84. PMID 7387872.
  4. Gladman DD, Antoni C, Mease P, Clegg DO, Nash P (2005). "Psoriatic arthritis: epidemiology, clinical features, course, and outcome". Ann. Rheum. Dis. 64 Suppl 2: ii14–7. doi:10.1136/ard.2004.032482. PMC 1766874. PMID 15708927.
  5. [1] Psoriasis Triggers at Psoriasis Net. 9-28-05. American Academy of Dermatology, 2008.
  6. Behnam SM, Behnam SE, Koo JY (2005). "Smoking and psoriasis". Skinmed. 4 (3): 174–6. PMID 15891254.
  7. [2][3] 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.
  8. Ortonne JP, Lebwohl M, Em Griffiths C (2003). "Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis". Eur J Dermatol. 13 (2): 117–23. PMID 12695125.
  9. Austin LM, Ozawa M, Kikuchi T, Walters IB, Krueger JG. "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". J. Invest. Dermatol. 113 (5): 752–9. doi:10.1046/j.1523-1747.1999.00749.x. PMID 10571730.
  10. [4] 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.
  11. Nickoloff BJ, Nestle FO (2004). "Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities". J. Clin. Invest. 113 (12): 1664–75. doi:10.1172/JCI22147. PMC 420513. PMID 15199399.

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