The adaptor molecule MyD88 activates PI-3 kinase signaling in CD4+ T cells and enables CpG oligodeoxynucleotide-mediated costimulation.

@article{Gelman2006TheAM,
  title={The adaptor molecule MyD88 activates PI-3 kinase signaling in CD4+ T cells and enables CpG oligodeoxynucleotide-mediated costimulation.},
  author={Andrew E. Gelman and David F Larosa and Jidong Zhang and Patrick T Walsh and Yongwon Choi and Jorge Sunyer and Laurence A Turka},
  journal={Immunity},
  year={2006},
  volume={25 5},
  pages={783-93}
}
While T cells respond directly to toll-like receptor (TLR) agonists, TLR-signaling pathways in T cells are poorly characterized. Here we demonstrate in CD4(+) T cells that CpG DNA directly enhances proliferation, prevents anergy, and augments humoral responses to a T cell-dependent antigen by a Myeloid differentiation primary-response protein 88 (MyD88) and Phosphatidylinositol 3-kinase (PI-3 kinase)-dependent pathway. PI-3 kinase activation required a putative Src-homology domain (SH2) binding… CONTINUE READING
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