| First Author | McKenzie GJ | Year | 1998 |
| Journal | Immunity | Volume | 9 |
| Issue | 3 | Pages | 423-32 |
| PubMed ID | 9768762 | Mgi Jnum | J:67965 |
| Mgi Id | MGI:1931799 | Doi | 10.1016/s1074-7613(00)80625-1 |
| Citation | McKenzie GJ, et al. (1998) Impaired development of Th2 cells in IL-13-deficient mice. Immunity 9(3):423-32 |
| abstractText | 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. |
