| First Author | Cheekatla SS | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 8 | Pages | 2815-2822 |
| PubMed ID | 28855309 | Mgi Jnum | J:251074 |
| Mgi Id | MGI:6103664 | Doi | 10.4049/jimmunol.1601231 |
| Citation | Cheekatla SS, et al. (2017) IL-21 Receptor Signaling Is Essential for Optimal CD4(+) T Cell Function and Control of Mycobacterium tuberculosis Infection in Mice. J Immunol 199(8):2815-2822 |
| abstractText | In this study, we determined the role of IL-21R signaling in Mycobacterium tuberculosis infection, using IL-21R knockout (KO) mice. A total of 50% of M. tuberculosis H37Rv-infected IL-21R KO mice died in 6 mo compared with no deaths in infected wild type (WT) mice. M. tuberculosis-infected IL-21R KO mice had enhanced bacterial burden and reduced infiltration of Ag-specific T cells in lungs compared with M. tuberculosis-infected WT mice. Ag-specific T cells from the lungs of M. tuberculosis-infected IL-21R KO mice had increased expression of T cell inhibitory receptors, reduced expression of chemokine receptors, proliferated less, and produced less IFN- gamma, compared with Ag-specific T cells from the lungs of M. tuberculosis-infected WT mice. T cells from M. tuberculosis-infected IL-21R KO mice were unable to induce optimal macrophage responses to M. tuberculosis. This may be due to a decrease in the Ag-specific T cell population. We also found that IL-21R signaling is associated with reduced expression of a transcriptional factor Eomesodermin and enhanced functional capacity of Ag-specific T cells of M. tuberculosis-infected mice. The sum of our findings suggests that IL-21R signaling is essential for the optimal control of M. tuberculosis infection. |
