| First Author | Skyberg JA | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 7 | Pages | e21978 |
| PubMed ID | 21765931 | Mgi Jnum | J:174937 |
| Mgi Id | MGI:5141540 | Doi | 10.1371/journal.pone.0021978 |
| Citation | Skyberg JA, et al. (2011) Murine and bovine gammadelta T cells enhance innate immunity against Brucella abortus infections. PLoS One 6(7):e21978 |
| abstractText | gammadelta T cells have been postulated to act as a first line of defense against infectious agents, particularly intracellular pathogens, representing an important link between the innate and adaptive immune responses. Human gammadelta T cells expand in the blood of brucellosis patients and are active against Brucella in vitro. However, the role of gammadelta T cells in vivo during experimental brucellosis has not been studied. Here we report TCRdelta(-/-) mice are more susceptible to B. abortus infection than C57BL/6 mice at one week post-infection as measured by splenic colonization and splenomegaly. An increase in TCRgammadelta cells was observed in the spleens of B. abortus-infected C57BL/6 mice, which peaked at two weeks post-infection and occurred concomitantly with diminished brucellae. gammadelta T cells were the major source of IL-17 following infection and also produced IFN-gamma. Depletion of gammadelta T cells from C57BL/6, IL-17Ralpha(-/-), and GMCSF(-/-) mice enhanced susceptibility to B. abortus infection although this susceptibility was unaltered in the mutant mice; however, when gammadelta T cells were depleted from IFN-gamma(-/-) mice, enhanced susceptibility was observed. Neutralization of gammadelta T cells in the absence of TNF-alpha did not further impair immunity. In the absence of TNF-alpha or gammadelta T cells, B. abortus-infected mice showed enhanced IFN-gamma, suggesting that they augmented production to compensate for the loss of gammadelta T cells and/or TNF-alpha. While the protective role of gammadelta T cells was TNF-alpha-dependent, gammadelta T cells were not the major source of TNF-alpha and activation of gammadelta T cells following B. abortus infection was TNF-alpha-independent. Additionally, bovine TCRgammadelta cells were found to respond rapidly to B. abortus infection upon co-culture with autologous macrophages and could impair the intramacrophage replication of B. abortus via IFN-gamma. Collectively, these results demonstrate gammadelta T cells are important for early protection to B. abortus infections. |
