[HTML][HTML] Skin innate immune system in psoriasis: friend or foe?

BJ Nickoloff - The Journal of clinical investigation, 1999 - Am Soc Clin Investig
BJ Nickoloff
The Journal of clinical investigation, 1999Am Soc Clin Investig
Clinical photograph of extensive psoriatic plaque formation with protective shield-like
appearance encircling the trunk, arms, and lower back/buttocks. granular cell layer,
elongation of rete pegs, or an angiogenic tissue reaction, are not present (10). Thus, as
current dogma now suggests, the barrier defect in psoriasis more likely represents a
consequence, rather than a cause, of infiltration by activated immunocytes that release
cytokines that trigger an aberrant differentiation program in the epidermis (11). Second …
Clinical photograph of extensive psoriatic plaque formation with protective shield-like appearance encircling the trunk, arms, and lower back/buttocks. granular cell layer, elongation of rete pegs, or an angiogenic tissue reaction, are not present (10). Thus, as current dogma now suggests, the barrier defect in psoriasis more likely represents a consequence, rather than a cause, of infiltration by activated immunocytes that release cytokines that trigger an aberrant differentiation program in the epidermis (11). Second, many drugs that selectively target activated T cells are very effective in producing remissions in psoriasis patients (12). Third, after an upper respiratory infection, psoriatic patients will develop numerous skin lesions that do not represent primary cutaneous infections. As discussed below, this finding suggests that activated immunocytes responsive to the initial bacterial infection can exit the pharynx and migrate to skin where they produce Th1-type cytokines (11).
Similarly, transgenic mice that constitutively produce gamma interferon (IFN-γ) in the epidermis, display profound barrier defects in the skin (13); intradermal injection of IFN-γ can also trigger psoriatic lesions in genetically susceptible patients (14). Interestingly, the altered keratin profile seen in keratin 10 knockout mice with disrupted barrier includes aberrant expression of keratin 17, which is also characteristically present in psoriatic plaques (15) and can be induced by exposure to IFN-γ either in-vivo (13) or in-vitro (16).
The Journal of Clinical Investigation