IL-2 limits IL-12 enhanced lymphocyte proliferation during Leishmania amazonensis infection

Amanda E. Ramer-Tait, Christine A. Petersen, Douglas E. Jones

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


C3H mice infected with Leishmania amazonensis develop persistent, localized lesions with high parasite loads. During infection, memory/effector CD44hiCD4+ T cells proliferate and produce IL-2, but do not polarize to a known effector phenotype. Previous studies have demonstrated IL-12 is insufficient to skew these antigen-responsive T cells to a functional Th1 response. To determine the mechanism of this IL-12 unresponsiveness, we used an in vitro assay of repeated antigen activation. Memory/effector CD44hiCD4+ T cells did not increase proliferation in response to either IL-2 or IL-12, although these cytokines upregulated CD25 expression. Neutralization of IL-2 enhanced CD4+ T cell proliferation in response to IL-12. This cross-regulation of IL-12 responsiveness by IL-2 was confirmed in vivo by treatment with anti-IL-2 antibodies and IL-12 during antigen challenge of previously infected mice. These results suggest that during chronic infection with L. amazonensis, IL-2 plays a dominant, immunosuppressive role independent of identifiable conventional Treg cells.

Original languageEnglish (US)
Pages (from-to)32-39
Number of pages8
JournalCellular Immunology
Issue number1
StatePublished - 2011
Externally publishedYes


  • IL-12
  • IL-2
  • Leishmania
  • T cell
  • Tolerance

ASJC Scopus subject areas

  • Immunology


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