IL-2 controls trafficking receptor gene expression and Th2 response for skin and lung inflammation

Both Il2−/− mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung inflammation. In contrast, Sf.Il2−/− double mutant mice do not display skin inflammation and markedly reduced lung inflammation. In this review, we summarize our recent findings based on microarray, q-PCR and functional studies of 10 Sf double mutant mice. These studies revealed novel pro-inflammatory functions of IL-2 in regulating inflammation in an organ-specific manner. IL-2 exerts its “organ-specific” pro-inflammatory function by regulating the migration and retention of CD4+ T-cells (both Th1 and Th2) specifically to the skin and lung. In addition, IL-2 is also required for regulating the Th2 cytokine response during T-cell activation. Further studies on these IL-2‐regulated genes will help in identifying novel targets for intervention in inflammatory diseases of skin and lung.

► IL‐2 is an inflammatory cytokine for skin and lung as well as T‐cell growth. ► Th1 cytokine and related TRGs are insufficient to induce skin and lung inflammation. ► IL‐2 is required for the expression of many of the Th2 related traffic genes. ► IL-2 controls the expression of the adhesion molecule ITGAE, CD103.