| First Author | Maciag K | Year | 2024 |
| Journal | J Immunol | Volume | 213 |
| Issue | 3 | Pages | 339-346 |
| PubMed ID | 38912839 | Mgi Jnum | J:361324 |
| Mgi Id | MGI:7711472 | Doi | 10.4049/jimmunol.2400145 |
| Citation | Maciag K, et al. (2024) Reappraising the Role of T Cell-Derived IFN-gamma in Restriction of Mycobacterium tuberculosis in the Murine Lung. J Immunol 213(3):339-346 |
| abstractText | T cells producing IFN-gamma have long been considered a stalwart for immune protection against Mycobacterium tuberculosis (Mtb), but their relative importance to pulmonary immunity has been challenged by murine studies that achieved protection by adoptively transferred Mtb-specific IFN-gamma-/- T cells. Using IFN-gamma-/- T cell chimeric mice and adoptive transfer of IFN-gamma-/- T cells into TCRbeta-/-delta-/- mice, we demonstrate that control of lung Mtb burden is in fact dependent on T cell-derived IFN-gamma, and, furthermore, mice selectively deficient in T cell-derived IFN-gamma develop exacerbated disease compared with T cell-deficient control animals, despite equivalent lung bacterial burdens. Deficiency in T cell-derived IFN-gamma skews infected and bystander monocyte-derived macrophages to an alternative M2 phenotype and promotes neutrophil and eosinophil influx. Our studies support an important role for T cell-derived IFN-gamma in pulmonary immunity against tuberculosis. |
