TCell Reactivation

Following transmigration from the circulation into dermal and epidermal tissue, memory T cells are brought into contact with antigen-presenting dendritic and Lan-gerhanscells, aswellaswithkeratinocytes, which, probably due to genetic alterations, are also able to act as APCs. This interaction leads to the re-activation of T cells and is followed by increased production and secretion of cytokines, including IL-2, IFN-y and TNF-a, which show the TH-1 cytokine pattern typically observed in psoriasis.

• IFN-y leads to induction of ICAM-1 in keratinocy-tes and endothelium, and consequently supports binding of lymphocytes to keratinocytes. TNF- induces keratinocyte proliferation and stimulates keratinocyte-induced interleukin-8 (IL-8) production. This leads to chemotaxis of lymphocytes and neutrophils into the epidermis. TNF- is also able to induce activation and proliferation of endothelial cells.

However, the exact mechanism by which (re-)activated T cells cause psoriatic lesions is not known. Direct lym phocyte/keratinocyte interactions could be involved, or cytokines produced during T-cell re-activation may be responsible for the most prominent alteration in psoriatic skin: hyperproliferation.

In summary, a combination of different mechanisms may be responsible for the changes observed histologi-cally and clinically in psoriatic skin. These include:

• Increased proliferation of keratinocytes (hyperker-atosis)

Neutrophil and mast-cell migration into epidermis and dermis, respectively

• Increased production of defensins by activated keratinocytes

Increased angiogenesis

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