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TLR1/2 signaling enhances CD8+T cell function and its underlying mechanism
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Abstract:
Objective:To investigate the effect of Toll like receptor 1/2(TLR1/2) signaling on CD8+T cells derived from 3LL tumor-bearing mice and its underlying mechanisms. Methods:3LL Lewis lung carcinoma cell line was used to establish tumor-bearing mice model, of which CD8+T cells were purified from the spleen by MACS. CD8+T cells were stimulated in vitro with PBS or TLR1/2 agonist, BLP, and then the gene and protein expression levels of TLRs in CD8+T cells were measured by Real-time PCR and Flow cytometry. What’s more, cytokine secretion and proliferation of CD8+T cells after PBS or BLP stimulation were detected by ELISA and Flow cytometry. The inhibitors of key signal molecules were used to explore the underlying mechanisms of BLP influencing CD8+T cells derived from 3LL-bearing mice. Results: Compared with PBS group, BLP not only greatly increased the expressions of TLR1 and TLR2 genes (TLR1: \[0.353±0.015\] vs \[0.101±0017\], P<0.01; TLR2: (\[0.232±0.031\] vs \[0.080±0.004\], P<0.05) and proteins (P<0.05), but also significantly enhanced the functional cytokine secretion (IFN-γ: \[2 375±305\] vs \[850±50\], P<0.05；IL-2: \[1 600±200\] vs \[350±50\]，P<0.05); in addition, it promoted the proliferation of CD8+T cells (P<0.05). All of these were dependent on NF-κB and P38 pathways. Conclusion: TLR1/2 signaling could directly promote the functions of CD8+T cells derived from 3LL-tumor bearing mice, which might enrich the scope of TLRs and also provide the basis for TLR agonist-based tumor immunotherapy.
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Project Supported:
Project supported by the National Natural Science Foundation of China (No. 31570892, No. 31400772)
Clc Number:
