T cell-intrinsic factors contribute to the differential ability of CD8 + T cells to rapidly secrete IFN-γ in the absence of antigen

Elsa N. Bou Ghanem, Christina C. Nelson, Sarah E.F. D'Orazio

Research output: Contribution to journalArticlepeer-review

19 Scopus citations

Abstract

A subset of CD44hiCD8+ T cells isolated from C57BL/6/J (B6) mice, but not BALB/c/By/J (BALB/c) mice, rapidly secrete IFN-γ 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-γ. Furthermore, BALB/c CD8+ T cells did not rapidly secrete IFN-γ 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 CD44hiCD8+ 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.

Original languageEnglish
Pages (from-to)1703-1712
Number of pages10
JournalJournal of Immunology
Volume186
Issue number3
DOIs
StatePublished - Feb 1 2011

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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