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Review
. 1999 Nov;104(9):1161-4.
doi: 10.1172/JCI8633.

Skin innate immune system in psoriasis: friend or foe?

B J Nickoloff  1
Affiliations
Review

Skin innate immune system in psoriasis: friend or foe?

B J Nickoloff. J Clin Invest. 1999 Nov.
No abstract available

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Figures

Figure 1
Figure 1
Clinical photograph of extensive psoriatic plaque formation with protective shield-like appearance encircling the trunk, arms, and lower back/buttocks.
Figure 2
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
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.
See this image and copyright information in PMC

Comment on

References

    1. Farber EM, Nall LM. The natural history of psoriasis in 5600 patients. Dermatologica. 1974;148:1–18. - PubMed
    1. Vyse TJ, Todd JA. Genetic analysis of autoimmune disease. Cell. 1996;85:311–318. - PubMed
    1. Travers JB, et al. Epidermal HLA-DR and the enhancement of cutaneous reactivity to superantigenic toxins in psoriasis. J Clin Invest. 1999;104:1181–1189. - PMC - PubMed
    1. Elias, P.M., et al. 1993. Normal mechanisms and pathophysiology of epidermal permeability barrier homeostasis. Curr. Opin. Dermatol. 231–237.
    1. Tsai J-C, et al. Permeability barrier disruption alters the localization and expression of TNF-alpha protein in the epidermis. Arch Dermatol Res. 1996;286:242–248. - PubMed