Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Finkelman, F.D. et al.

Finkelman, Yang, Perkins, Schleifer, Sproles, Santeliz, Bernstein, Rothenberg, Morris, Wills-Karp,

Suppressive effect of IL-4 on IL-13-induced genes in mouse lung.

Although IL-4 signals through two receptors, IL-4R alpha/common gamma-chain (gamma(c)) and IL-4R alpha/IL-13R alpha1, and only the latter is also activated by IL-13, IL-13 contributes more than IL-4 to goblet cell hyperplasia and airway hyperresponsiveness in murine asthma. To determine whether unique gene induction by IL-13 might contribute to its greater proasthmatic effects, mice were inoculated intratracheally with IL-4 or IL-13, and pulmonary gene induction was compared by gene microarray and real-time PCR. Only the collagen alpha2 type VI (Ca2T6) gene and three small proline-rich protein (SPRR) genes were reproducibly induced > 4-fold more by IL-13 than by IL-4. Preferential IL-13 gene induction was not attributable to B cells, T cells, or differences in cytokine potency. IL-4 signaling through IL-4R alpha/gamma(c) suppresses Ca2T6 and SPRR gene expression in normal mice and induces these genes in RAG2/gamma(c)-deficient mice. Although IL-4, but not IL-13, induces IL-12 and IFN-gamma, which suppress many effects of IL-4, IL-12 suppresses only the Ca2T6 gene, and IL-4-induced IFN-gamma production does not suppress the Ca2T6 or SPRR genes. Thus, IL-4 induces genes in addition to IL-12 that suppress STAT6-mediated SPRR gene induction. These results provide a potential explanation for the dominant role of IL-13 in induction of goblet cell hyperplasia and airway hyperresponsiveness in asthma.[1]

References

Suppressive effect of IL-4 on IL-13-induced genes in mouse lung. Finkelman, F.D., Yang, M., Perkins, C., Schleifer, K., Sproles, A., Santeliz, J., Bernstein, J.A., Rothenberg, M.E., Morris, S.C., Wills-Karp, M. J. Immunol. (2005) [Pubmed]

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