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&z.ast;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.
| Original language | English |
|---|---|
| Pages (from-to) | 876-886 |
| Number of pages | 11 |
| Journal | Human Vaccines and Immunotherapeutics |
| Volume | 10 |
| Issue number | 4 |
| DOIs | |
| State | Published - Apr 1 2014 |
Keywords
- Biologic therapies
- Cytokine inhibitors
- IL-17
- IL-22
- IL-23
- Immunotherapy
- Interleukins
- Psoriasis
- TNF-α
- Vaccines
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