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[|There is no formal proof that
neutrophils do maintain psoriasis, since there is no way to block them specifically. What we do know from much more
targeted therapies is that blocking T-cells or the APC-T-cells interaction
reverses psoriasis lesions, and thus it is much more likely to speculate that the adoptive immune system maintains

The first inflammatory cell studied for its role in psoriasis was the neutrophil. The neutrophil is attracted and activated beneath the stratum corneum by numerous chemotactic substances. Some are chemokines secreted by the keratinocytes and activated T lymphocytes, others are fractions of the complement cascade and clotting factors that come along and self-activate on contact with the stratum corneum. Once locally activated, the neutrophils release their lysosomal enzymes, causing tissue damage and, more specifically, a chronic tissue damage in the subcorneal region, leading to never-ending epidermal healing. [Inhibiting migration of the neutrophils causes the psoriasis plaques to disappear|I do not agree with this statement. Indeed
virtually all antipsoriatic treatments have been shown to inhibit the migration
of neutrophils in vivo. However, some treatments with a powerful effect on
neutrophil migration are ineffective in psoriasis such as leukotriene B4
receptor antagonist, topical 13-cis-retinoic acid and dapsone. van de Kerkhof PCM. The polymorphonuclear leukocytes in: Psoriasis.
Reonigk HH and Maiback eds. New York, Marcel Dekker Inc 1998:209-25

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