1. Program in Molecular Pathogenesis, Helen L. and Martin S. Kimmel Center for Biology and Medicine, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, USA
2. Department of Immunology and Microbial Sciences, The Scripps Research Institute, La Jolla, California 92037, USA
3. These authors contributed equally to this work.

Correspondence to: Michael L. Dustin¹Dorian B. McGavern² Correspondence and requests for materials should be addressed to M.L.D. (Email: dustin@saturn.med.nyu.edu) and D.B.M. (Email: mcgad@scripps.edu).

Lymphocytic choriomeningitis virus¹ infection of the mouse central nervous system (CNS) elicits fatal immunopathology through blood–brain barrier breakdown² and convulsive seizures³. Although lymphocytic-choriomeningitis-virus-specific cytotoxic T lymphocytes (CTLs) are essential for disease⁴, their mechanism of action is not known. To gain insights into disease pathogenesis, we observed the dynamics of immune cells in the meninges by two-photon microscopy. Here we report visualization of motile CTLs and massive secondary recruitment of pathogenic monocytes and neutrophils that were required for vascular leakage and acute lethality. CTLs expressed multiple chemoattractants capable of recruiting myelomonocytic cells. We conclude that a CD8⁺ T-cell-dependent disorder can proceed in the absence of direct T-cell effector mechanisms and rely instead on CTL-recruited myelomonocytic cells.