Abstract Recent studies indicate tissue-resident memory CD8 T cells (Trms) form at both the sites of initial infection and in lymphoid tissues upon resolution of systemic or localized viral infections. We examined if lymph node Trms were also generated in lung-draining mediastinal lymph nodes (mLN) during intranasal infections. Both transgenic P14 cells and endogenous influenza-specific CD69+/CD103+ Trms were detected in lung-draining mLN but absent in non-draining LNs after intranasal infection with recombinant influenza or vaccinia viruses. Similar to lung Trms, which wane over time, these primary memory (1M) mLN Trms had limited persistence with continual contraction throughout the memory phase. As influenza is a seasonal virus, and we previously observed that repeated antigen exposure extended the durability of lung Trms, we investigated the effects of multiple antigen exposures on the mLN Trm population. Similar to their lung Trm-counterparts, the lung-draining LN Trms derived from repeatedly stimulated (4M) memory CD8 T cells exhibited extended survival, down-regulation of Eomesodermin and the shared IL-2/15Rβ CD122 compared to 1M LN Trms. During parabiosis, both 1M and 4M mLN Trms largely maintained residence within their respective hosts. Importantly, hosts containing 4M P14 mLN Trms provided superior early protection against LCMV challenge in the mLN compared to 1M hosts, demonstrating the functional capacity for mLN Trms to contribute to protective anti-viral immune responses. Overall, these data indicate that lung-draining lymph node Trms co-express CD69 and CD103, largely maintain LN-tissue residency and can contribute to subsequent viral infections.