Impaired development of Th2 cells in IL-13-deficient mice.
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 RIS Download
Animals | B-Lymphocytes | CD4-Positive T-Lymphocytes | Cell Differentiation | Drug Resistance | Gene Targeting | Immunization | Immunoglobulin E | Interleukin-13 | Interleukin-4 | Interleukin-5 | Mast Cells | Mice | Mice, Inbred C57BL | Mice, Knockout | Mutagenesis, Insertional | Nematode Infections | Neomycin | Phosphoglycerate Kinase | Receptors, IgE | Recombinant Proteins | Spleen | Th2 Cells