Cytokine Secretion by γδ and αβ T cells in Monophasic Experimental Autoimmune Encephalomyelitis

γδ T Cells Express Activation Markers in the Central Nervous System of Mice with Chronic-relapsing Experimental Autoimmune Encephalomyelitis

“…In contrast, IL-4 secreting T cells in spleen increased as disease resolved. Our data are in substantial agreement with results of Jensen et al [19], with a higher percentage of T cells staining positive for IFN-than in the corresponding TCR + population and relatively few cells reactive for IL-4. We also did not find that T cells secreted IL-2 (data not shown).…”

“…CD62L is also rapidly shed following activation with inflammatory mediators [22], and thus decreased expression of this marker at the height of clinical disease may also reflect a response to increased presence of these factors in the CNS. Analysis of the classical activation marker, CD25, also showed elevated expression on T cells in the CNS, particularly during early phases of the disease, an observation consistent with a role for these cells in the development of a proinflammatory environment within the CNS, as has been demonstrated in depletion studies [17,18], and cytokine analyses of T cells isolated from lesions [19]. In contrast to the data for CD25, CD62L and CD69, expression of CD122 and CD95/CD95L on T cells was remarkably different from that found on total lymphocytes.…”

“…Analysis of cytokine production of T cells in EAE by Jensen and colleagues [19] would also be supportive of the contribution of different populations of T cells to disease expression. In their studies, IFN--secreting T cells were markedly enriched in lymphoid organs at disease onset and comprised a large percentage of the cytokine-secreting T cell population in both the CNS and lymphoid organs during active stages.…”

“…Of particular note are the studies of Jensen and colleagues using an ELISPOT assay where they showed that T cells comprise 20% of the total IFN--secreting cells in the CNS at disease onset, rising to 40% at height of disease. In contrast, IL-4 secreting T cells in the spleen were found to be low at disease onset, but increased as disease evolved [19].…”

γ/δ T Cell-Deficient Mice Exhibit Reduced Disease Severity and Decreased Inflammatory Response in the Brain in Murine Neurocysticercosis

“…In the brain, ␥␦ T cells have been identified at the margins of chronic multiple sclerosis plaques, and they appeared to become the prevalent type of T cell (46). Similarly, ␥␦ T cells were found in the CNS during EAE (47). Although the role of ␥␦ T cells in the pathogenesis of EAE appears controversial (48 -51), studies of ␥␦ T cell-depleted mice suggest that ␥␦ T cells contribute in the pathogenesis of EAE by regulating the influx of inflammatory cells and augmenting the proinflammatory cytokine profile in the brain (50,51).…”