| First Author | Wohler JE | Year | 2009 |
| Journal | Eur J Immunol | Volume | 39 |
| Issue | 6 | Pages | 1516-26 |
| PubMed ID | 19384874 | Mgi Jnum | J:149481 |
| Mgi Id | MGI:3848587 | Doi | 10.1002/eji.200839176 |
| Citation | Wohler JE, et al. (2009) Gammadelta T cells in EAE: early trafficking events and cytokine requirements. Eur J Immunol 39(6):1516-26 |
| abstractText | We have previously shown that gammadelta T cells traffic to the CNS during EAE with concurrently increased expression of beta(2)-integrins and production of IFN-gamma and TNF-alpha. To extend these studies, we transferred bioluminescent gammadelta T cells to WT mice and followed their movement through the acute stages of disease. We found that gammadelta T cells rapidly migrated to the site of myelin oligodendrocyte glycoprotein peptide injection and underwent massive expansion. Within 6 days after EAE induction, bioluminescent gammadelta T cells were found in the spinal cord and brain, peaking in number between days 10 and 12 and then rapidly declining by day 15. Reconstitution of gammadelta T cell(-/-) mice with gammadelta T cells derived from beta(2)-integrin-deficient mice (CD11a, -b or -c) demonstrated that gammadelta T-cell trafficking to the CNS during EAE is independent of this family of adhesion molecules. We also examined the role of gammadelta T-cell-produced IFN-gamma and TNF-alpha in EAE and found that production of both cytokines by gammadelta T cells was required for full development of EAE. These results indicate that gammadelta T cells are critical for the development of EAE and suggest a therapeutic target in demyelinating disease. |
