Experimental autoimmune uveoretinitis (EAU) serves as an animal model for human uveitis. EAU is inducible in animals by peripheral immunization with proteins found in the retina that triggers an immune response which leads to tissue damage. This is coordinated by autoantigen specific CD4(+) T cells whose activation is accompanied by the infiltration of a wide range of other leukocytes into the retina. Infiltrating macrophages and granulocytes cause destruction by the release of reactive oxygen and nitrogen species but these and other leukocytes also regulate inflammation. This review will describe the dynamics of leukocyte infiltration in EAU from the initial systemic activation of T cells following immunization, through their traffic into the eye causing a peak of infiltration, and ending with a phase of secondary regulation in which, although clinical disease has resolved, the leukocyte composition of the eye remains altered.