Psoriasis and Susceptibility to Other Autoimmune Diseases

An Outline for the Clinician

Faisal R Ali; Richard B Warren


Expert Rev Clin Immunol. 2013;9(2):99-101. 

In This Article


While GWAS have disclosed many new genetic associations of psoriasis, our understanding of causative mutations remains incomplete. The phenomenon of linkage disequilibrium, in which adjacent sections of the genome appear to be inherited together, prevents us from definitively attributing mutations of a particular base pair to susceptibility to psoriasis. This is exemplified by the well-recognized PSORS1 susceptibility region that encodes HLA-C.[6] Future work will be focused around fine mapping of such autoimmune susceptibility regions to better inform our understanding of precise causation.

There will also be a commensurate increase in functional studies of associated molecular pathways in the pathogenesis of psoriasis to provide further therapeutic strategies. For example, IL-17, identified by GWAS as being strongly associated with psoriasis, has been successfully targeted by monoclonal antibodies in promising Phase II trials.[19,20]

Furthermore, our greater understanding of pharmacogenetics, the relationship between genetic susceptibility markers and response to therapy, will usher in a new era of stratified medicine, in which an individual's genetic profile will be used to guide initial therapy to both maximize efficacy and reduce the likelihood of toxicity.[21]

As greater numbers of patients with psoriasis are treated with systemic and biologic agents, our epidemiological knowledge of the safety and longer-term side effects of such medications will increase. In the next 5–10 years psoriasis-specific data will be available from dermatologic registries, such as the British Association of Dermatologists Biologics Interventions Register.[22]