Senescent cells develop in response to cellular stress and can contribute to cancer and degenerative diseases by driving chronic tissue inflammation. This study shows that CD4+ T cells can remove senescent fibroblasts by recognizing an antigen derived from human cytomegalovirus (HCMV), a herpesvirus that establishes lifelong latent infections in most humans. The authors compared skin samples from younger (aged 16–28) and older (aged 53–74) female donors and showed that senescent cells were increased in the older skin compared with in the younger cohort, but they did not detect any further age-associated accumulation within the older group. This suggested that senescent cells were being actively removed from the skin. The authors found perforin+ CD4+ T cells are increased in older compared with younger skin and that their numbers negatively correlated with senescent cell numbers. These cytotoxic CD4+ T cells induced apoptosis in senescent fibroblasts in an MHC-II-dependent manner. HCMV was shown to become reactivated in senescent fibroblasts, leading to the presentation of the HCMV-derived glycoprotein B on MHC-II molecules, which were targeted by specific CD4+ T cells to induce apoptosis in the senescent cells. The authors propose that HCMV may serve a commensal-like role in facilitating the immunosurveillance of senescent cells.