CD8⁺ T cells are critical for the long term protection against intracellular pathogens. Upon resolution of an infection a small number of activated CD8⁺ T cells can persist long term as circulating central and effector memory T cells, or as non-migratory tissue resident memory T cells at the site of infection. Collectively these memory subsets establish a widespread state of surveillance which can rapidly provide protection against re-infection. Understanding and identifying the migratory cues which affect the development, function and maintenance of these CD8⁺ memory T cells subsets could contribute to the development of effective viral vaccines. Our preliminary studies have shown that memory CD8⁺ T cells express high levels of the inflammatory chemokine receptor CCR2 and that loss of this receptor results in reduced memory cell numbers following influenza infection. This loss of memory was not restricted to any specific memory subset but represented an equivalent reduction in the generation of all circulating and resident memory cell subsets, suggesting a general defect in cell maintenance.  Loss of CCR2 deficient CD8⁺ memory cells following viral clearance was associated with altered spatio-temporal distribution within secondary lymphoid organs. We have identified a potential macrophage – chemokine network within secondary lymphoid organs that may contribute to the maintenance of CD8⁺ memory T cells following viral infection and explain the loss of CCR2 deficient CD8⁺ memory cells. Using clodronate loaded liposomes we have specifically depleted lymph node macrophages following influenza infection to determine their role in supporting CD8⁺ T cell maintenance after the clearance of infection.