Evolutionary regulation of human Fas ligand (CD95L) by plasmin in solid cancer immunotherapy



Summary

Human Fas ligand (CD95L) is a key player in immune cell-mediated killing of cancer cells. However, cancer cells can manipulate FasL to evade the immune system. This research explores how the enzyme plasmin, often elevated in solid tumors, regulates FasL activity. Plasmin cleaves FasL, altering its signaling properties and potentially impacting its ability to induce cell death. This interaction presents a complex regulatory mechanism in the tumor microenvironment. Understanding this interplay between plasmin and FasL is crucial for optimizing solid cancer immunotherapy strategies by influencing tumor sensitivity to FasL-mediated killing and preventing immune evasion. Modulation of plasmin activity or FasL modification could enhance immunotherapy efficacy.

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