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.
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.
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.
Within the immune system, the development of psoriasis is based upon four key pathways/interactions:
↑[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.
↑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. PMID10571730.CS1 maint: Multiple names: authors list (link)
↑[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.