PI3Kδ drives the pathogenesis of experimental autoimmune encephalomyelitis by inhibiting effector T cell apoptosis and promoting Th17 differentiation.

@article{HaylockJacobs2011PI3KDT,
  title={PI3Kδ drives the pathogenesis of experimental autoimmune encephalomyelitis by inhibiting effector T cell apoptosis and promoting Th17 differentiation.},
  author={Sarah Haylock-Jacobs and Iain Comerford and Mark D. Bunting and Ervin E. Kara and Scott L. Townley and Manuela Klingler-Hoffmann and Bart Vanhaesebroeck and Kamal D. Puri and Shaun R McColl},
  journal={Journal of autoimmunity},
  year={2011},
  volume={36 3-4},
  pages={
          278-87
        }
}
The Class IA phosphoinositide 3-kinase delta (PI3Kδ) has been implicated in multiple signaling pathways involved in leukocyte activation and hence is an attractive target in many human autoimmune diseases, including multiple sclerosis (MS). Here, using mice expressing a catalytically inactive form of the PI3Kδ subunit p110δ, we show that signaling through PI3Kδ is required for full and sustained pathology of experimental autoimmune encephalomyelitis (EAE), a Th17-driven model of MS. In p110… CONTINUE READING
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