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An interleukin 4 (IL-4)-independent pathway for CD4+ T cell IL-4 production is revealed in IL-4 receptor-deficient mice.

IL-4 receptor alpha chain (IL-4Ralpha)-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-4Ralpha 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 IL-4Ralpha-/- mice were isolated by cell sorting. Upon primary stimulation by T cell receptor cross-linkage, the CD62L-low, but not the CD62L-high, cells secreted considerable amounts of IL-4, which was strikingly enhanced upon 4-day culture with anti-CD3 in the presence or absence of IL-4. CD62L-low cells isolated from IL-4Ralpha-/-, beta2-microglobulin-/- double homozygous mice produced less IL-4 than did either IL-4Ralpha-/- or wild-type mice. These results indicate that an IL-4-independent, beta2-microglobulin-dependent pathway exists through which the CD62L-low CD4+ population has acquired IL-4-producing capacity in vivo, strongly suggesting that these cells are NK T cells.

Pubmed ID: 9380721


  • Noben-Trauth N
  • Shultz LD
  • Brombacher F
  • Urban JF
  • Gu H
  • Paul WE


Proceedings of the National Academy of Sciences of the United States of America

Publication Data

September 30, 1997

Associated Grants

  • Agency: NCI NIH HHS, Id: CA20408

Mesh Terms

  • Animals
  • CD4-Positive T-Lymphocytes
  • Gene Targeting
  • Interleukin-4
  • Mice
  • Mice, Inbred BALB C
  • Mice, Mutant Strains
  • Receptors, Interleukin-4
  • Th2 Cells
  • beta 2-Microglobulin