Lesional psoriatic T cells contain the capacity to induce a T cell activation molecule CDw60 on normal keratinocytes.

In this report we demonstrate, that in psoriatic skin, basal and suprabasal keratinocytes express CDw60. The CDw60-specific monoclonal antibody, UM4D4, has recently been shown to recognize the 9-O-acetylated disialosyl group on ganglioside GD3. The CDw60 antigen on cultured keratinocytes also seems to be identical with the 9-O-acetylated disialosyl group, because the anti-UM4D4 binding was markedly reduced after neuraminidase treatment of keratinocytes. To examine whether factors from T cells in psoriatic lesions are responsible for the overexpression of CDw60 on keratinocytes, T cell lines obtained from lesional skin were initiated and cloned by limiting dilution. Factors released from 19 of 19 activated T cell clones up-regulated CDw60 expression on cultured normal keratinocytes. T-cell-secreted cytokines, including interleukin (IL)-2, IL-3, IL-4, IL-6, IL-13, transforming growth factor-beta, granulocyte/macrophage colony-stimulating factor, and interferon-gamma were tested for their capacity to modulate keratinocyte CDw60 expression. IL-4 and IL-13 strongly up-regulated the expression of CDw60; by contrast, interferon-gamma down-regulated keratinocyte CDw60 expression. Interestingly, IL-13 may in part be responsible for the T-cell-induced up-regulation of CDw60, because anti-IL-13 partly neutralized this effect of the T cell supernatant. In conclusion, CDw60 expression on psoriatic epidermal keratinocytes is likely induced by intralesionally activated T cells and may in part be due to IL-13. These findings would represent a novel mechanism by which T cells participate in the pathogenesis of psoriasis.