| First Author | Green AM | Year | 2013 |
| Journal | J Immunol | Volume | 190 |
| Issue | 1 | Pages | 270-7 |
| PubMed ID | 23233724 | Mgi Jnum | J:190810 |
| Mgi Id | MGI:5449752 | Doi | 10.4049/jimmunol.1200061 |
| Citation | Green AM, et al. (2013) IFN-gamma from CD4 T Cells Is Essential for Host Survival and Enhances CD8 T Cell Function during Mycobacterium tuberculosis Infection. J Immunol 190(1):270-7 |
| abstractText | IFN-gamma is necessary in both humans and mice for control of Mycobacterium tuberculosis. CD4 T cells are a significant source of IFN-gamma during acute infection in mice and are required for control of bacterial growth and host survival. However, several other types of cells can and do produce IFN-gamma during the course of the infection. We sought to determine whether IFN-gamma from sources other than CD4 T cells was sufficient to control M. tuberculosis infection and whether CD4 T cells had a role in addition to IFN-gamma production. To investigate the role of IFN-gamma from CD4 T cells, a murine adoptive transfer model was developed in which all cells were capable of producing IFN-gamma, with the exception of CD4 T cells. Our data in this system support that CD4 T cells are essential for control of infection, but also that IFN-gamma from CD4 T cells is necessary for host survival and optimal long-term control of bacterial burden. In addition, IFN-gamma from CD4 T cells was required for a robust CD8 T cell response. IFN-gamma from T cells inhibited intracellular replication of M. tuberculosis in macrophages, suggesting IFN-gamma may be necessary for intracellular bactericidal activity. Thus, although CD4 T cells play additional roles in the control of M. tuberculosis infection, IFN-gamma is a major function by which these cells participate in resistance to tuberculosis. |
