Skin innate immune system in psoriasis: friend or foe? - PubMed (original) (raw)
Review
. 1999 Nov;104(9):1161-4.
doi: 10.1172/JCI8633.
Affiliations
- PMID: 10545511
- PMCID: PMC409832
- DOI: 10.1172/JCI8633
Review
Skin innate immune system in psoriasis: friend or foe?
B J Nickoloff. J Clin Invest. 1999 Nov.
No abstract available
Figures
Figure 1
Clinical photograph of extensive psoriatic plaque formation with protective shield-like appearance encircling the trunk, arms, and lower back/buttocks.
Figure 2
Schematic representation depicting how a confederacy of innate immunity-based genes and cells may conspire to create a psoriatic lesion. Whether triggered by an exogenous event that disrupts KC barrier function (with or without bacterial infection) or by an endogenously-derived infiltration of activated immunocytes, the final mature psoriatic plaque includes an epidermal compartment resistant to infections, apoptosis, and transformation. The complexity of interactions between innate immunity and acquired immunity in skin is depicted as a multi-step model highlighting 2 key abnormalities in psoriasis, including (a) defective terminal differentiation/barrier function and (b) hyperreactivity of the skin immune system including T cells bearing NKRs, which can evolve into a full-fledged Th1-type cell-mediated reaction involving adaptive immune components.
Figure 3
Potential means to reverse the hyperresponsiveness of psoriatic skin. Possible intervention points based on a multistep model of psoriasis, beginning with inflammatory-type reactions involving innate immunity and culminating in acquired immunity and activation of an angiogenic switch.
Comment on
- Epidermal HLA-DR and the enhancement of cutaneous reactivity to superantigenic toxins in psoriasis.
Travers JB, Hamid QA, Norris DA, Kuhn C, Giorno RC, Schlievert PM, Farmer ER, Leung DY. Travers JB, et al. J Clin Invest. 1999 Nov;104(9):1181-9. doi: 10.1172/JCI6835. J Clin Invest. 1999. PMID: 10545517 Free PMC article. Clinical Trial.
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