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Discussion
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* intact CD58:CD2 interaction necessary for anti-tumor immunity
* Defects in this axis lead to multi-faceted immune evasion through impaired CD2-dependent T cell polyfunctionality, T cell exclusion, impaired intra-tumoral proliferation, & concurrent protein stabilization of PD-L1
* 2 potential therapeutic avenues, including rescued activation of human CD2-expressing tumor-infiltrating lymphocytes using recombinant CD58 protein, & targeted disruption of PD-L1/CMTM6 interactions