Depletion and Decreased Function of Antigen-Presenting Dendritic Cells Caused by Lymphocytapheresis in Ulcerative colitis

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Abstract
The therapeutic efficacy of lymphocytapheresis in autoimmune diseases is presumed to be caused by depletion of activated lymphocytes. However, nothing is known about the inducer of activated lymphocytes, the antigen-presenting dendritic cells, during lymphocytapheresis. Six sessions of lymphocytapheresis were done in five patients with ulcerative colitis. Dendritic cells were enriched from the buffy coat of depleted lymphocytes and also from the peripheral blood. The phenotype and function of dendritic cells were studied by dual-color flow cytometry and in allogenic mixed leukocyte reaction, respectively. The serum levels of inflammatory cytokines (interleukin-1α 6, 8, 10, and 12 and tumor necrosis factor-α and β) were measured before and after lymphocytapheresis in all cases. Lymphocytapheresis was safe and caused clinical, endoscopic or histologic improvements in all patients with ulcerative colitis. Many CD83-positive mature dendritic cells were found in the buffy coats after each session of lymphocytapheresis. The function of dendritic cells, the frequencies of CD83-positive dendritic cells and the levels of interleukin-6 and interleukin-8 were down regulated in all patients with ulcerative colitis after lymphocytapheresis compared with their levels before lymphocytapheresis. Depletion and down regulation of the function of dendritic cells and diminished levels of inflammatory cytokines caused by lymphocytapheresis may contribute to the therapeutic efficacy of lymphocytapheresis.

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