Which immunologic factors are associated with psoriasis?

Updated: Nov 20, 2020
  • Author: Jacquiline Habashy, DO, MSc; Chief Editor: William D James, MD  more...
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Answer

Evidence suggests that psoriasis is an autoimmune disease. Studies show high levels of dermal and circulating TNF-α. Treatment with TNF-α inhibitors is often successful. Psoriatic lesions are associated with increased activity of T cells in the underlying skin.

Psoriasis is related to excess T-cell activity. Experimental models can be induced by stimulation with streptococcal superantigen, which cross-reacts with dermal collagen. This small peptide has been shown to cause increased activity among T cells in patients with psoriasis but not in control groups. Some of the newer drugs used to treat severe psoriasis directly modify the function of lymphocytes.

Also of significance is that 2.5% of those with HIV develop worsening psoriasis with decreasing CD4 counts. This is paradoxical, in that the leading hypothesis on the pathogenesis of psoriasis supports T-cell hyperactivity and treatments geared to reduce T-cell counts help reduce psoriasis severity. This finding is possibly explained by a decrease in CD4 T cells, which leads to overactivity of CD8 T cells, which drives the worsening psoriasis. The HIV genome may drive keratinocyte proliferation directly.

HIV associated with opportunistic infections may see increased frequency of superantigen exposure leading to similar cascades as above mentioned.

Guttate psoriasis often appears following certain immunologically active events, such as streptococcal pharyngitis, cessation of steroid therapy, and use of antimalarial drugs.


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