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 PMID:9768762  

Impaired development of Th2 cells in IL-13-deficient mice.

G J McKenzie | C L Emson | S E Bell | S Anderson | P Fallon | G Zurawski | R Murray | R Grencis | A N McKenzie
Immunity | 1998

We report that Th2 cell cultures generated using T cells or splenocytes from IL-13-deficient mice produce significantly reduced levels of IL-4, IL-5, and IL-10 compared with wild-type. In contrast, IL-4 and IL-5 production by mast cells stimulated in vitro with PMA, ionomycin, or IgE cross-linking are unaffected. In vitro Th2 cell differentiation cannot be rescued by the addition of exogenous factors, but in vivo antigen challenge and administration of IL-13 can increase Th2-like cytokine responses as can infection with the parasitic nematode Nippostrongylus brasiliensis. IL-13-deficient mice also have lower basal levels of serum IgE and biased antigen-specific immunoglobulin responses. Thus, IL-13 is an important regulator of Th2 commitment and may therefore play a central role in atopy and infectious diseases.

Pubmed ID: 9768762

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Associated grants

  • Agency: Wellcome Trust, United Kingdom

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