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Sir, Tumour necrosis factor α (TNF-α) is a proven adequate target for treatment of psoriasis. The chimeric TNF-α antibody infliximab binds to the transmembrane receptors and induces a neutralizing effect on soluble TNF by reversed signalling, ultimately causing a reduction in lesional T cells and, indirectly, increased programmed cell death of keratinocytes (1). CD26/dipeptidylpeptidase IV (DPPIV) is a multifunctional glycoprotein known to be present and upregulated on the surface of keratinocytes and T cells in psoriatic skin compared with the skin of healthy volunteers (2). The expression of CD26/DPPIV on peripheral blood T-lymphocytes of untreated psoriatic patients, however, was found to be substantially reduced, in particular on the CD8+CD26bright subset (3). Furthermore, TNF-α has been reported to influence CD26/DPPIV expression (4, 5). In vitro cell cultures have shown that anti-TNF-α can upregulate the expression of CD26/DPPIV on human-activated lymphocytes (6). CD26/DPPIV expression may have a crucial role and might function as a marker correlating with disease activity in the pathogenesis of psoriasis. The objective of this study was therefore to determine whether antiTNF-α therapy with infliximab modulates CD26/DPPIV expression on keratinocytes and T cells.

Persistent Expression of CD26/DPPIV After Treatment with Infliximab in Psoriasis Despite Clinical Improvement