KLRG1, is upregulated on aged or chronically stimulated T cells and transmits inhibitory signals that limit proliferation and effector functions. Ulviprubart’s blockade of KLRG1 aims to rejuvenate T cell responses, enhance cytokine production, and improve immune-mediated clearance of tumors or persistent pathogens. Its IgG1 isotype may also engage Fc-dependent effector mechanisms to deplete KLRG1-positive suppressive cells, offering a dual strategy to overcome immune exhaustion in age-related or chronic diseases.