Canadian Health&Care; Mall

Allergic airway inflammation is an important characteristic of atopic asthma. Proinflammatory cells, including antigen-presenting cells (APCs), eosinophils, mast cells, basophils and lymphocytes contribute to the development and persistence of the inflammation . There is evidence that the T helper (Th)2-type cytokines such as interleukin (IL)-4 or IL-5 have a role in the pathogenenesis of asthma . By contrast, the Th1-type cytokine interferon (IFN)-y has an antiallergic role . However, recent studies showing that passive transfer of ovalbumin (OVA)-specific, Th1-skewed, CD4+ T cells into OVA-sensitized mice failed to attenuate, but rather exacerbated, airway inflammation after OVA challenge have made it difficult to understand the asthmatic inflammation based on the simple counterbalance theory of Th1 versus Th2 . Thus, both Th1- and Th2-skewed responses in asthmatics may be regulated by more complex mechanisms than previously estimated. These mechanisms likely involve regulatory cytokines, including tranforming growth factor-beta and IL-10 . IL-10 is a pleiotrophic cytokine released from various types of cells, including lymphocytes, mast cells, eosinophils and monocytes/macrophages . While IL-10 was originally isolated as a cytokine selectively produced from Th2-cells and shown to inhibit Th1-skewed response in mice , it is now appreciated that not only Th2 cells, but also Th1 cells, potentially produce IL-10 in humans . IL-10 inhibits the production of proinflammatory cytokines from T cells directly and indirectly through inhibition of the antigen-presenting functions of APCs . Furthermore, IL-10 downregulates proinflam-matory cytokines and chemokine production by granulocytes, and inhibits the survival of eosinophils . By contrast, IL-10 enhances B cell maturation into plasma cells . Thus, except for this proinflammatory effect on B cells, the major role of IL-10 in atopic diseases is postulated to act as a damp-ener of inflammation as a feedback mechanism .