The meningeal lymphatic network – housed within the dural meninges surrounding the brain – represents a critical pathway enabling cerebrospinal fluid (CSF) drainage. By facilitating CSF drainage, this network enables the removal of central nervous system (CNS) waste and enables immunological recognition of brain and spinal cord-derived antigens. During aging and in Alzheimer’s disease (AD), a failure of functional meningeal lymphatic drainage promotes toxic misfolded protein build up – including amyloid beta – and attenuates effective CNS antigen surveillance. Thus, alleviation of age-related meningeal lymphatic dysfunction represents a promising therapeutic strategy to alleviate AD pathology, however, the mechanisms underlying this decline remain elusive. Here we demonstrate that age-related alterations in meningeal immunity – driven by functional changes in diverse stromal populations – contribute to meningeal lymphatic impairment. Dura aging and in AD, elevated dural vascular adhesion molecules and excessive fibrosis promote enhanced T cell recruitment and retention in the dural meninges, predominantly associated with Th1 and Th2 phenotypes. Single-cell RNA-sequencing of dural lymphatic endothelial cells in aged mice demonstrates signatures associated with responsiveness to T cell-derived cytokines, particularly IFN-γ and IL-4, representing key Th1 and Th2-derived cytokines respectively. Chronic elevation of IFN-γ and IL-4 in the CSF and dural meninges of young mice via AAV-mediated overexpression promotes impaired CSF drainage to deep cervical lymph nodes by altering lymphatic junctions - comparable to that observed in aged mice – and precipitating lymphatic vessel hyperpermeability. Conversely, IFN-y and IL-4 blockade in aged mice alleviated age-related impairments in meningeal lymphatic function. These data suggest manipulation of meningeal immunity as a viable therapeutic target to normalize CSF drainage in aged mice and alleviate pathology in AD mice associated with impaired waste removal.