Aside from the typical symptoms of haemorrhagic disease, Dengue is increasingly reported as associated with neurological complications, including dengue encephalitis, although the pathogenic mechanisms underlying the complications remain unclear. We therefore investigated this in C57BL/6 mice, intracranially infected via the postglenoid foramen with non-adapted dengue virus 2. Trafficking of leukocytes was evaluated by histological, 18-parameter flow cytometric and mRNA analysis of the brain, cervical lymph nodes (CLN), spleen, bone marrow, and blood at various timepoints post infection (p.i.). There were significantly more infiltrating effector CD8+ T cells (GrB+CD62Llow CCR7low IL7R-αint-low), GrB+CD69+ NK cells, myeloid DC (MHC-IIhi CD11chi CD8- CD4-/+ CD11b+) and inflammatory Ly6Chi macrophages in the brains of infected mice than those of the mock-infected group, but with different kinetics for each subset. NK and CD8+ T cells peaked at d6 and d9 p.i., respectively, correlating with the increased intracellular granzyme B (GrB) and perforin mRNA expression, while leukocyte recruitment correlated with increased CCL5, CCL2, CCL3, CXCL10, CXCR3, TNF-α as well as IFN-γmRNA expression observed at d6 p.i. Intriguingly, intracerebral accumulation of T cells and DC, but not NK cells was significantly impaired after cervical lymphadenectomy. On CLN T lymphocytes, CD62L decreased from d3 to d9, but recovering by d13 p.i.,. These findings suggest infiltrating CD69+ NK and effector CD8+ T cells contribute to viral eradication via a GrB-dependent mechanism at early and later phases, respectively, in resistant mice. The significant reduction of intracerebral infiltrating T cells and the kinetics of CD62L shedding on CLN T lymphocytes reveals a crucial role of the draining CLN as a reservoir for infiltrating CD8+ T cells.