Knockout of FGL1 in Tumor Cell Lines Leads to Decreased Binding Between MHC II and LAG 3

Lung cancer is the most lethal cancer with the highest mortality rate. However, because of developed resistance from patients, certain drugs for lung cancer treatment have displayed inadequate effects in enhancing prognosis. Recent studies show that the cause of resistance might be due to inhibited T Cell proliferation that results from the binding of LAG 3 with its two ligands, FGL1 and MHC II. Therefore, because the two ligands interact with LAG 3 on the same domains, and the two ligand's both inhibit T Cell proliferation, the binding of one ligand may alter the binding of the other ligand to LAG 3. In this study, we explore the effect of FGL1 knockout on MHC II and LAG 3 binding. The results of this study will provide insight into whether FGL1 increases/decreases MHC II and LAG 3 interaction. Hence, by understanding this mechanism, treatment would be able to alter T Cell proliferation by regulating FGL1 which could lead to improved prognosis in patients.