| First Author | Seixas EM | Year | 1999 |
| Journal | J Immunol | Volume | 162 |
| Issue | 5 | Pages | 2837-41 |
| PubMed ID | 10072531 | Mgi Jnum | J:124535 |
| Mgi Id | MGI:3721835 | Doi | 10.4049/jimmunol.162.5.2837 |
| Citation | Seixas EM, et al. (1999) gammadelta T cells contribute to control of chronic parasitemia in Plasmodium chabaudi infections in mice. J Immunol 162(5):2837-41 |
| abstractText | During a primary infection of mice with Plasmodium chabaudi, gammadelta T cells are stimulated and their expansion coincides with recovery from the acute phase of infection in normal mice or with chronic infections in B cell-deficient mice (mu-MT). To determine whether the large gammadelta T cell pool observed in female B cell-deficient mice is responsible for controlling the chronic infection, studies were done using double-knockout mice deficient in both B and gammadelta cells (mu-MT x delta-/-TCR) and in gammadelta T cell-depleted mu-MT mice. In both types of gammadelta T cell-deficient mice, the early parasitemia following the peak of infection was exacerbated, and the chronic parasitemia was maintained at significantly higher levels in the absence of gammadelta T cells. The majority of gammadelta T cells in C57BL/6 and mu-MT mice responding to infection belonged predominantly to a single family of gammadelta T cells with TCR composed of Vgamma2Vdelta4 chains and which produced IFN-gamma rather than IL-4. |
