Interleukin 25 in allergic airway inflammation.
T helper 2 (Th2) cells induce allergic inflammation through the production of cytokines such as interleukin (IL)-4, IL-5 and IL-13. Recently, it has been demonstrated that a novel IL-17 family cytokine IL-25 ( IL-17E) is a product of activated Th2 cells and mast cells. Interestingly, when systemically administered to mice, IL-25 induces IL-4, IL-5 and IL-13 production from undefined non-T/non-B cells and then induces Th2-type immune responses such as blood eosinophilia and increased serum immunoglobulin E levels. In addition, we have recently shown that IL-25 mRNA is expressed in the lung after an inhaled antigen challenge in sensitized mice and that neutralization of the produced IL-25 by soluble IL-25 receptor decreases antigen-induced eosinophil and CD4+ T cell recruitment into the airways. Moreover, we have shown that the enforced expression of IL-25 in the lung significantly enhances antigen- induced Th2 cytokine production and eosinophil recruitment into the airways, and that the IL-25-mediated enhancement of antigen-induced eosinophil recruitment is inhibited by the depletion of CD4+ T cells. Thus, it is suggested that IL-25 plays an important role in enhancing allergic airway inflammation by a CD4+ T-cell-dependent mechanism.[1]References
- Interleukin 25 in allergic airway inflammation. Tamachi, T., Maezawa, Y., Ikeda, K., Iwamoto, I., Nakajima, H. Int. Arch. Allergy Immunol. (2006) [Pubmed]
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