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176 discovered that AHR probably functions as a key transcription factor in regulating CD8 + T cell exhaustion, such that in exhausted CD8 + T cells, inhibition of AHR activity or knockdown of AHR leads to the down‐regulation of PD‐1, TIM‐3, LAG‐3 and CD39, whereas IFN‐γ and TNF are up‐regulated
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doi: 10.1016/j.hermed.2020.100382 97
and in plasma and erythrocyte lysates
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