| First Author | Bou Ghanem EN | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 3 | Pages | 1703-12 |
| PubMed ID | 21191063 | Mgi Jnum | J:168908 |
| Mgi Id | MGI:4939291 | Doi | 10.4049/jimmunol.1001960 |
| Citation | Bou Ghanem EN, et al. (2011) T cell-intrinsic factors contribute to the differential ability of CD8+ T cells to rapidly secrete IFN-gamma in the absence of antigen. J Immunol 186(3):1703-12 |
| abstractText | A subset of CD44(hi)CD8(+) T cells isolated from C57BL/6/J (B6) mice, but not BALB/c/By/J (BALB/c) mice, rapidly secrete IFN-gamma within 16 h of infection with Listeria monocytogenes. This Ag-independent response requires the presence of both IL-12 and IL-18. Previous studies showed that dendritic cells from B6 mice produced more Th1-type cytokines such as IL-12 than did those from BALB/c mice in response to L. monocytogenes infection. In this report, we demonstrate that the microenvironment in L. monocytogenes-infected BALB/c mice is sufficient to induce responsive B6 CD8(+) T cells to rapidly secrete IFN-gamma. Furthermore, BALB/c CD8(+) T cells did not rapidly secrete IFN-gamma even when they were exposed to high concentrations of IL-12 plus IL-18 in vitro. In the presence of IL-12 and IL-18, B6 CD44(hi)CD8(+) T cells upregulated expression of the receptor subunits for these cytokines more rapidly than did BALB/c T cells. In comparing particular subsets of memory phenotype CD8(+) T cells, we found that virtual memory cells, rather than true Ag-experienced cells, had the greatest level of impairment in BALB/c mice. These data suggest that the degree of cytokine-driven bystander activation of CD8(+) T cells that occurs during infection depends on both APCs and T cell-intrinsic properties that can vary among mouse strains. |
