Loss of β2-integrin function results in metabolic reprogramming of dendritic cells, leading to increased dendritic cell functionality and anti-tumor responses.

Here, we found that Akt and mTOR signaling were upregulated in cells expressing dysfunctional β2-integrins ( Figure 4a ), and there was a trend toward increased iNOS expression in these cells, although the results did not reach statistical significance ( Figure 4c ).

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