Human CCL27/CTACK ELISA Kit

Background Skin-infiltrating T cells play a predominant role in allergic and inflammatory skin diseases such as atopic dermatitis and allergic contact dermatitis. These T cells are attracted by chemotactic factors, e.g. RANTES (regulation on activation, normal T cell expressed and secreted; CCL5), TARC (thymus and activation regulated chemokine; CCL17) and CTACK (cutaneous T-cell attracting chemokine; CCL27). Objectives To investigate which T-cell-attracting chemokines are involved in allergic contact dermatitis in mice. Methods Allergic contact dermatitis was induced by application of dinitrochlorobenzene (DNCB) or toluene-2,4-diisocyanate (TDI), and chemokine concentrations were determined by enzyme-linked immunosorbent assay. The effects on chemokine concentrations of the highly selective phosphodiesterase 4 inhibitor cilomilast and the glucocorticoid diflorasone diacetate were studied in mouse ears. Results RANTES and TARC were elevated in both models of allergic contact dermatitis 24 h after challenge, whereas CTACK remained unchanged. The increase in RANTES was diminished in mouse ears pretreated with cilomilast or diflorasone diacetate. TARC was reduced by diflorasone diacetate in the DNCB model but was highly induced in the TDI model; in contrast, TARC was not influenced by cilomilast. Conclusions TARC and RANTES, but not CTACK, are involved in these two models of allergic contact dermatitis.

Background: Drug-induced skin reactions, including toxic epidermal necrolysis and Stevens-Johnson syndrome, are severe buttons cutaneous diseases of uncertain etiology, although cytotoxic T cells seem to be involved. Cutaneous T cell-attracting chemokine (CTACK/CCL27) is selectively expressed in skin and attracts CCR10-expressing cells. Exclusive CTACK expression by keratinocytes; suggests its involvement in inflammatory skin diseases. Objective: We addressed whether CTACK/CCL27 production by the epidermis and CCR10(+) lymphocytes are involved in toxic epidermal necrolysis and Stevens-Johnson syndrome. Methods: We measured CTACK expression by epidermal cells in 2 patients with drug-induced buttons skin reactions and compared it to lesional skin from several drug-induced exanthemas. In parallel we measured CCR10 mRNA in peripheral blood mononuclear cells from the patients during the course of the disease and in lymphocytes infiltrating the skin. Results: CTACK expression levels in skin biopsies from the 2 patients with drug-induced buttons reactions were higher than those found in healthy subjects or in other drug-induced exanthemas. CCR10 mRNA levels were also elevated in peripheral blood lymphocytes and in lesional skin during the acute phase of the disease. Moreover, resolution was associated with a return to baseline of both CTACK and CCR10 receptor expression. Conclusion: CTACK-CCR10 interactions may be involved in the selective recruitment to the skin of cytotoxic lymphocytes in toxic epidermal necrolysis and Stevens-Johnson syndrome, as well as in less severe drug-induced cutaneous diseases.