Interleukin-13 (IL-13) is secreted by many cell types, but especially T helper type 2 (Th2) cells. IL-13 is an important mediator of allergic inflammation and disease. In addition to effects on immune cells, IL-13 is implicated as a central mediator of the physiologic changes induced by allergic inflammation in many tissues.
The functions of IL-13 overlap considerably with those of IL-4, especially with regard to changes induced on hematopoietic cells, but these effects are probably less important given the more potent role of IL-4. Thus, although IL-13 can induce immunoglobulin E (IgE) secretion from activated human B cells, deletion of IL-13 from mice does not markedly affect either Th2 cell development or antigen-specific IgE responses induced by potent allergens. In comparison, deletion of IL-4 abrogates these responses. Thus, rather than a lymphoid cytokine, IL-13 acts more prominently as a molecular bridge linking allergic inflammatory cells to the non-immune cells in contact with them, thereby altering physiological function.