Figure 1. Model of the relationship between skin and joint inflammation.

Genes with variants (box) contributing to psoriasis and/or psoriatic arthritis susceptibility. While infiltrating leukocytes and their cytokine products are currently better characterized in the skin than in the inflamed joint, they may be similar in both sites. Leukocytes and cytokines originating in the skin may play a direct or indirect role in the development of arthritis. Alternatively, they may originate in the synovium in a similar manner to their development in the skin.

Gene variants (blue boxes) that predispose to psoriasis influence pro-inflammatory pathways, notably the Th1 and Th17 pathways. Model of cytokine networks in psoriasis adapted from Lowes, MA et al, 2007. The role of the 5q31 region harboring IL4/IL13 is speculative at this stage. HBD (beta defensin) is upregulated in keratinocytes as a result of stimulation by IL20 and other cytokines. An increase in the number of copies of gene family members is also associated with psoriasis.