In:
Immunology, Wiley, Vol. 145, No. 2 ( 2015-06), p. 225-231
Abstract:
The control of Trypanosoma cruzi infection is related to interferon‐ γ ( IFN ‐ γ ) activation leading to intracellular clearance of parasites. The transcription factor signal transducer and activator of transcription 1 ( STAT ‐1) is a key mediator of IFN ‐ γ intracellular signalling and knockout of this protein leads to susceptibility to several intracellular microbes. To determine the role of STAT ‐1 in host susceptibility to T. cruzi infection we compared the survival, parasite loads and balance of IFN ‐ γ and interleukin‐10 ( IL ‐10) responses between wild‐type and STAT ‐1 knockout mice. We found that the lack of STAT ‐1 resulted in a more robust infection, leading to higher levels of blood and tissue parasites and markedly reduced survival. In addition, infected STAT ‐1 knockout mice had higher systemic levels of both IFN ‐ γ and IL ‐10, suggesting that the absence of STAT ‐1 leads to a disequilibrium of pro‐inflammatory and anti‐inflammatory cytokines. Analysis of spleen cells indicates that CD 4, CD 8 cells generate IFN ‐ γ and natural killer cells express IL ‐13 in STAT ‐1 knockout animals. The production of IL ‐17 is particularly enhanced in the absence STAT ‐1 expression but did not reduce mortality. Overall these results indicate that STAT ‐1 is important for the control of T. cruzi infection in mice.
Type of Medium:
Online Resource
ISSN:
0019-2805
,
1365-2567
DOI:
10.1111/imm.2015.145.issue-2
Language:
English
Publisher:
Wiley
Publication Date:
2015
detail.hit.zdb_id:
2006481-0
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