Journal article
IL-2 limits IL-12 enhanced lymphocyte proliferation during Leishmania amazonensis infection
Cellular immunology, Vol.270(1), pp.32-39
2011
DOI: 10.1016/j.cellimm.2011.03.016
PMCID: PMC3129441
PMID: 21481338
Abstract
C3H mice infected with
Leishmania amazonensis develop persistent, localized lesions with high parasite loads. During infection, memory/effector CD44
hiCD4
+ 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 CD44
hiCD4
+ 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 T
reg cells.
Details
- Title: Subtitle
- IL-2 limits IL-12 enhanced lymphocyte proliferation during Leishmania amazonensis infection
- Creators
- Amanda E Ramer-TaitChristine A PetersenDouglas E Jones
- Resource Type
- Journal article
- Publication Details
- Cellular immunology, Vol.270(1), pp.32-39
- DOI
- 10.1016/j.cellimm.2011.03.016
- PMID
- 21481338
- PMCID
- PMC3129441
- NLM abbreviation
- Cell Immunol
- ISSN
- 0008-8749
- eISSN
- 1090-2163
- Publisher
- Elsevier Inc
- Language
- English
- Date published
- 2011
- Academic Unit
- Epidemiology; Internal Medicine
- Record Identifier
- 9983996092502771
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