Not just another kinase: the many roles of PI3K-δ in adaptive immunity

Le résumé fourni par la source

PI3K transmit signals from receptors by phosphorylating phosphoinositides on the inner leaflet of the plasma membrane. PI3K enzymatic activity was first described by Lewis Cantley and colleagues in the late 1980s.1 This triggered a race to clone the genes for these enzymes. The last such to be reported was the gene for PI3K-δ (PIK3CD), reported independently by 2 groups in 1997.2,3 PI3Kδ is one of 4 class I PI3Ks—all of which have in common that they generate the second-messenger signaling molecule PIP3 in response to tyrosine kinase (PI3Kα, PI3Kβ, and PI3Kδ) and/or GPCR (PI3Kβ and PI3Kγ) signaling.4 PI3K was initially shown to be engaged by CD19 and CD28, which have motifs similar to the PDGFR and insulin receptor in their cytoplasmic domains.5,6 While PI3K engagement by CD19 is essential for its capacity to provide activation signals to B cells,7 CD28 can provide costimulation independently of PI3K,8 which instead is essential for the related costimulatory receptor ICOS.9 It later became evident that both the BCR and TCR engage directly with PI3Kδ through mechanisms that remain to be fully elucidated.10

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.