| First Author | Tatari-Calderone Z | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 9 | Pages | 5629-36 |
| PubMed ID | 16237052 | Mgi Jnum | J:119360 |
| Mgi Id | MGI:3701901 | Doi | 10.4049/jimmunol.175.9.5629 |
| Citation | Tatari-Calderone Z, et al. (2005) CD4-dependent signaling is required for a late checkpoint during Th2 development associated with resistance to activation-induced cell death. J Immunol 175(9):5629-36 |
| abstractText | Previous studies have found that class II-restricted T cells from CD4-deficient mice reconstituted with a tail-less CD4 transgene have a specific defect in the development of Th2 effector cells; however, the reason for this defect was not clear. Following stimulation with a high potency peptide and exogenous IL-4, CD4-dependent signaling is required for optimal generation of a Th2 effector population. However, initial IL-4 and GATA-3 transcription is appropriately induced, suggesting that the initial stages of Th2 development are intact and independent of CD4 after priming with a strong agonist peptide. In addition to the defect in Th2 development, CD4 mutant T cells are also relatively resistant to activation-induced cell death (AICD). Furthermore, inhibition of AICD in wild-type T cells causes a defect in Th2 development similar to that seen in the CD4 mutant T cells. These data support the hypothesis that CD4-dependent signaling pathways regulate a distinct checkpoint in the expansion and commitment phase of Th2 development, which is related to dysregulation of AICD. |
