Caveat: Monoclonal antibodies 20.1 and 103.2 bind all human BTN3A proteins and are not suited to study BTN3A1-specific features
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The title of Zhou et al. (1) claims that “Up-regulation of BTN3A1 on CD14+ cells promotes V γ 9V δ 2 T cell activation in psoriasis.” The study nicely confirms in quite some detail that V γ 9V δ 2 T cells from psoriatic patients increasingly home to skin, produce higher amounts of IFN γ , TNF α
[1] Y. Kong,et al. MAP4-regulated dynein-dependent trafficking of BTN3A1 controls the TBK1–IRF3 signaling axis , 2016, Proceedings of the National Academy of Sciences.
[2] E. Adams,et al. The molecular basis for modulation of human V(gamma)9V(delta)2 T cell response by CD277/Butryophilin (BTN3A)-specific antibodies , 2012 .