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• W2103704908 abstract "Toll-like receptor (TLR) activation is primarily thought to affect antigen-presenting cells (APCs) by inducing an innate immune response that can subsequently activate the adaptive immune system. However, there are increasing data that demonstrate expression and activation of TLRs on T cells, thus providing evidence for a direct role for TLRs in the activation of an adaptive immune response. A study recently demonstrated that Pam3CSK { N -palmitoyl- S -[2,3-bis(palmitoloxy)-(2 RS )-propyl]-Cys-Ser-Lys 4 }, a TLR2 agonist lipopeptide, activates T helper 1 (T H 1) cells and induces interferon-γ (IFN-γ) production, even in the absence of TLR1, which differs from its mechanism of activation of APCs. Moreover, whereas Pam3CSK-stimulated IFN-γ production by T H 1 cells is ablated in the absence of both myeloid differentiation marker 88 (MyD88), an adaptor protein in the TLR pathway, and interleukin-1 receptor (IL-1R)–associated kinase–4 (IRAK4), the mitogen-activated protein kinases p38 and c-Jun N-terminal kinase (JNK) are still phosphorylated. These data suggest that TLR2 activation of T H 1 cells occurs through a mechanism different from that described for APCs and provides further evidence of direct TLR activation of the adaptive immune system." @default.
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• W2103704908 date "2007-09-04" @default.
• W2103704908 modified "2023-10-01" @default.
• W2103704908 title "T Cell Activation by TLRs: A Role for TLRs in the Adaptive Immune Response" @default.
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• W2103704908 doi "https://doi.org/10.1126/stke.4022007pe48" @default.
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