Lun_2007_J.Clin.Immunol_27_430

CD26, which is a costimulatory molecule and peptidase, is responsible for the degradation of interferon (IFN)-gamma-induced chemokines. To elucidate the immunopathological role of CD26 in allergic asthma, we investigated plasma soluble CD26 (sCD26) concentration and its cell surface expression on lymphocytes, monocytes, CD4+ T helper, CD8+ T suppressor plus cytotoxic T, invariant natural killer T (iNKT), and CD19+ B lymphocytes in allergic asthmatic patients. Plasma sCD26 was significantly elevated in asthmatic patients regardless of inhaled corticosteroid treatment (all P < 0.05). Cell surface expression of CD26 was significantly up-regulated on lymphocytes, especially on CD4+ and iNKT lymphocytes (all P < 0.05), but not on other cell types. Significant positive correlations were found between sCD26 and the percentage of eosinophils, Th2-related chemokines CCL5 and CCL22, and costimulatory molecule sCTLA-4 (all P < 0.05). In conclusion, the aberrant expression of CD26 may contribute to the inflammatory process and Th2 predominance in the immunopathogenesis of allergic asthma.