| First Author | Noben-Trauth N | Year | 1997 |
| Journal | Proc Natl Acad Sci U S A | Volume | 94 |
| Issue | 20 | Pages | 10838-43 |
| PubMed ID | 9380721 | Mgi Jnum | J:43656 |
| Mgi Id | MGI:1098188 | Doi | 10.1073/pnas.94.20.10838 |
| Citation | Noben-Trauth N, et al. (1997) An interleukin 4 (IL-4)-independent pathway for CD4+ T cell IL-4 production is revealed in IL-4 receptor-deficient mice. Proc Natl Acad Sci U S A 94(20):10838-43 |
| abstractText | IL-4 receptor alpha chain (IL-4R alpha)-deficient mice were generated by gene-targeting in BALB/c embryonic stem cells, Mutant mice showed a loss of IL-4 signal transduction and functional activity. The lack of IL-4R alpha resulted in markedly diminished, but not absent, TH2 responses after infection with the helminthic parasite Nippostrongylus brasiliensis. CD4(+), CD62L-high, and CD62L-low T cell populations from uninfected TL-4R alpha(- /-) mice were isolated by cell sorting, Upon primary stimulation by T cell receptor cross-linkage, the CD62L- low, bur not the CD62L-high, cells secreted considerable amounts of IL-4, which was strikingly enhanced upon 4-day culture with anti-CDS in the presence or absence of IL-4. CD62L-low cells isolated from IL-4R alpha(-/-), beta(2)- microglobulin(-/-) double homozygous mice produced less IL- 4 than did either IL-4R alpha(-/-) or wild-type mice. These results indicate that an IL-4-independent, beta(2)- microglobulin-dependent pathway exists through which tile CD62L-low CD4(+) population has acquired IL-4-producing capacity in vivo, strongly suggesting that these cells are NK T cells. |
