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NKG2D engagement induced the secretion of cytokines such as IFNγ and GM-CSF [58].
CD69 engagement induced TGFβ production by NK and T cells [63].
CD40 engagement induced high Bcl-XL protein expression in NOD as well as NOR Th40 cells.
Surprisingly, CD152 engagement induced activated Th1 cell migration towards CXCL12, CCL19, and CCL4, the ligands for CXCR4, CCR7, and CCR5, respectively, whereas inhibition of CD152 abrogated migration.
In contrast, TCR engagement induced comparable Ca2+ signaling in T cells purified from wild type and CD83Tg mice (figure 7C, 7D).
Again, this did not reflect a generalized defect in cellular calcium handling since TCR engagement induced comparable Ca2+ signaling in purified CD83Tg and wild-type T cells.
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PRR engagement induces production of proinflammatory cytokines such as TNF-α and IL-1β.
LFA-1 engagement induces transient activation of Rac1 and Rac2 in peripheral human T cells.
Moreover, in T cells FAK signaling downstream of fibronectin engagement induces MMP2 and MMP9 mRNA expression and protein release [56].
On the other hand, TCR engagement induces dephosphorylation of ERM proteins via Rac in T cells, which is proposed to enhance T cell interaction with APCs [30].
Through "inside-out" signaling, T cell receptor (TCR) engagement induces allosteric transition of LFA-1 to a high-affinity activation state.
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