| First Author | Cardona AE | Year | 2002 |
| Journal | J Immunol | Volume | 169 |
| Issue | 6 | Pages | 3163-71 |
| PubMed ID | 12218134 | Mgi Jnum | J:78958 |
| Mgi Id | MGI:2386524 | Doi | 10.4049/jimmunol.169.6.3163 |
| Citation | Cardona AE, et al. (2002) gamma/delta T Cell-Deficient Mice Exhibit Reduced Disease Severity and Decreased Inflammatory Response in the Brain in Murine Neurocysticercosis. J Immunol 169(6):3163-71 |
| abstractText | In a recently developed mouse model for neurocysticercosis, the immune response was characterized by a massive influx of gammadelta T cells and a type 1 pathway of cytokine expression. To understand the role of gammadelta T cells during this infection, the cellular and cytokine response was analyzed in mice that lack gammadelta T cells (TCRdelta(-/-)). In TCRdelta(-/-) mice, Mesocestoides corti metacestodes preferentially invaded the extraparenchymal areas of the brain. Furthermore, parasites were able to escape from the brain and establish a systemic infection with liver and peritoneal involvement. Immunopathological studies indicated that TCRdelta(-/-) mice develop little inflammatory response and less neurological symptomatology. Significantly reduced numbers of T cells, macrophages, dendritic cells, and mast cells were present in the brain. The cytokine response in the brain of TCRdelta(-/-) mice appears to be a mixed type1/type 2 response with low levels of IL-2, IL-4, IL-10, IL-12, IL-13, IL-15, and IFN-gamma. To further investigate the immunological significance of this cell population, gammadelta T cells were adoptively transferred into intracranially infected TCRdelta(-/-) mice. gammadelta T cells were specifically recruited into the CNS in response to this parasitic infection, and they were able to target the infected brain within 12 h after transfer. These results suggest that gammadelta T cells are key players in the immune response elicited during this CNS infection and direct a type 1 response in wild-type mice upon infection. |
