 
            IndraLab
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                                  "The mechanisms involved implies that CCL5 promotes the formation of the kappa-B p65/STAT3 complex, which activates COP9 signalosome 5 (CSN5) transcription, and then CSN5 further regulates the deubiquitination and stability of PD-L1, further inhibiting CD8+ T cell responses and thus leading to immune escape (67)(
Figure 1
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 In this study, our data provide evidence that menin promotes the ubiquitination and degradation of PD‐L1 by inhibiting the expression of the deubiquitinating enzyme CSN5, thereby decreasing the stability of PD‐L1 in cells.CTLA4 and PD‐L1/PD‐1 are usually activated in TME and repress T cell‐mediated cytotoxicity."