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Abstract
Psoriasis is a chronic, immune skin disease associated with significant morbidity. Development of psoriasis is influenced by numerous genes, one allele is HLA-CW*0602. Other genes and single nucleotide polymorphisms affect immunologic pathways and antimicrobial peptide synthesis. Dendritic cells initiate psoriasis by activating T-cells toward a Th1 and Th17 response, with increased cytokines including TNF-α, IL-6, -12, -17, -22, and -23. IL-22 appears to promote keratinocyte dedifferentiation and increased antimicrobial peptide synthesis while TNF-α and IL-17 induce leukocyte localization within the psoriatic plaque. These recent insights identifying key cytokine pathways have led to the development of inhibitors with significant efficacy in the treatment of psoriasis. While a strategy for vaccine modulation of the immune response in psoriasis is in progress, with new technology they may provide a cost-effective long-term treatment that may induce tolerance or targeted self-inhibition for patients with autoimmune disorders, such as psoriasis.
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Financial Disclosure
H.K.W. honoraria from Amgen. In addition, he is an investigator for Amgen, Janssen, Abbvie, and Celgene. All other authors report no conflicts of interest.
Funding
National Psoriasis Foundation grants to M.E.A., B.H.K., and H.K.W.
Acknowledgments
The authors would like to acknowledge the support of the National Psoriasis Foundation Grants to M.E.A., B.H.K., and H.K.W.