
Cross-talk between lactate metabolism and immunity reveals CEP55 as a potential regulator in the immunosuppressive microenvironment of hepatocellular carcinoma
The interaction of lactate metabolism with immunity plays a crucial role in the remodeling of the immune microenvironment and even in the heterogeneous progression of hepatocellular carcinoma (HCC). The intratumor-accumulated lactate served a vital role in the inefficacy of antitumor immune responses, the aggressiveness of tumor cells, and immunotherapy.1 Furthermore, lactate generated from the tumor microenvironment can be used as fuel for the proliferation and infiltration of immunosuppressive cells.2 Previous studies regarding the taxonomies of HCC, solely from the perspective of lactate3 or tumor immune microenvironment4 may introduce the potential for bias in the comprehension of HCC heterogeneity. Thus, deciphering the crosstalk properties between lactate and immune is imperative.