Cancer cells present aberrant glycosylation patterns that contribute to the evasion of antitumor immunity by triggering lectin receptors. Therefore, tumor glycosylation represents an interesting target for novel immunotherapy strategies. This review discusses the different mechanisms by which tumor-derived glycans induce tolerogenic programs in immune cells and their clinical significance.
ABSTRACT
Tumor immune escape refers to the process by which cancer cells evade detection and destruction by the immune system. Glycosylation, a post-translational modification that is altered in almost all cancer types, plays a crucial role in this process by modulating immune responses. This review examines our current understanding of how aberrant tumor glycosylation contributes to a tolerogenic microenvironment, focusing on specific glycosylation signatures—fucosylation, truncated O-glycans, and sialylation—and the immune receptors involved. Additionally, the clinical significance of tumor glycosylation is discussed, emphasizing its potential in developing novel therapeutic approaches aimed at improving immune system recognition and targeting of cancer cells. The review underscores the importance of ongoing research in this area to identify effective strategies for countering tumor immune escape and enhancing the efficacy of cancer treatments.