Upon anti-PD1 treatment a similar trend was observed in C57BL/6 J Nod2 fs mice transplanted with an alternative, less immunogenic syngeneic tumor cell-line, AT-3, although this did not reach statistical significance ( SI Appendix , Fig.
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Common inherited loss-of-function mutations in the innate sensor NOD2 contribute to exceptional immune response to cancer immunotherapy.
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A difficult question for future studies is how does NOD2 function as an immune tolerance checkpoint, either in the context of Crohn’s disease or immune reactions to cancer? In the context of the findings here, how does lower NOD2 signaling increase tumor infiltration with effector CD8 T cells and the therapeutic immune response to anti-PD-1? The role of NOD2 in sensing the large commensal population of gut bacteria seems likely to be significant, since germ free mice treated with anti-PD1 mount a poor immune response to MC38 tumor cells that is restored by a defined gut bacterial mixture, with the restored response dependent upon CD8 T cells ( 64 ).