Determination of Lymphocyte JAM-C Expression in Patients With Psoriasis Vulgaris

Psoriasis, Psoriasis Vulgaris

Psoriasis, JAM3 protein, human, Cell Adhesion Molecules, Skin, Inflammation, Lymphocytes

The stepwise process of leukocyte extravasation to inflamed tissues depends on the expression of a variety of cytokines and adhesion molecules. Recently much attention has focused on the Junctional Adhesion Molecules (JAM). The three members of this adhesion molecule family, namely, JAM-A, -B and -C, have been shown to govern the last step of leukocyte extravasation (transmigration) - the process of leukocytes passing between endothelial cells. In addition to transmigration, some members of this family seem to support additional steps in the leukocyte extravasation cascade. The investigators recently showed, that antibody-mediated inhibition of JAM-C significantly reduced hapten induced skin inflammation (J Invest Dermatol;125(5):969). Recent unpublished work from our laboratory showed, that JAM-C expression of lymphocytes can be up-regulated through specific activators. Hence, the investigators hypothesize, that JAM-C expression is elevated in patients with psoriasis. As it is currently not know, which factors may influence the expression of JAM-C, the investigators intend to analyse JAM-C expression on CD3+CD41- cells at several time-points during the treatment of psoriatic patients. Expression of JAM-C will then be correlated to disease activity (PASI).

The stepwise process of leukocyte extravasation to inflamed tissues depends on the expression of a variety of cytokines and adhesion molecules. Recently much attention has focused on the Junctional Adhesion Molecules (JAM). The three members of this adhesion molecule family, namely, JAM-A, -B and -C, have been shown to govern the last step of leukocyte extravasation (transmigration) - the process of leukocytes passing between endothelial cells. In addition to transmigration, some members of this family seem to support additional steps in the leukocyte extravasation cascade. We recently showed, that antibody-mediated inhibition of JAM-C significantly reduced hapten induced skin inflammation (J Invest Dermatol;125(5):969). Recent unpublished work from our laboratory showed, that JAM-C expression of lymphocytes can be up-regulated through specific activators. Hence, we hypothesize, that JAM-C expression is elevated in patients with psoriasis. As it is currently not know, which factors may influence the expression of JAM-C, we intend to analyse JAM-C expression on CD3+CD41- cells at several time-points during the treatment of psoriatic patients. Expression of JAM-C will then be correlated to disease activity (PASI). Detailed in- and exclusion criteria are outlined below.

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