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  4. Mice from a genetically resistant background lacking the interferon gamma receptor are susceptible to infection with Leishmania major but mount a polarized T helper cell 1-type CD4+ T cell response
 
research article

Mice from a genetically resistant background lacking the interferon gamma receptor are susceptible to infection with Leishmania major but mount a polarized T helper cell 1-type CD4+ T cell response

Swihart, K.
•
Fruth, U.
•
Messmer, N.
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1995
Journal of Experimental Medicine

Mice with homologous disruption of the gene coding for the ligand-binding chain of the interferon (IFN) gamma receptor and derived from a strain genetically resistant to infection with Leishmania major have been used to study further the role of this cytokine in the differentiation of functional CD4+ T cell subsets in vivo and resistance to infection. Wild-type 129/Sv/Ev mice are resistant to infection with this parasite, developing only small lesions, which resolve spontaneously within 6 wk. In contrast, mice lacking the IFN-gamma receptor develop large, progressing lesions. After infection, lymph nodes (LN) and spleens from both wild-type and knockout mice showed an expansion of CD4+ cells producing IFN-gamma as revealed by measuring IFN-gamma in supernatants of specifically stimulated CD4+ T cells, by enumerating IFN-gamma-producing T cells, and by Northern blot analysis of IFN-gamma transcripts. No biologically active interleukin (IL) 4 was detected in supernatants of in vitro-stimulated LN or spleen cells from infected wild-type or deficient mice. Reverse transcription polymerase chain reaction analysis with primers specific for IL-4 showed similar IL-4 message levels in LN from both types of mice. The IL-4 message levels observed were comparable to those found in similarly infected C57BL/6 mice and significantly lower than the levels found in BALB/c mice. Anti-IFN-gamma treatment of both types of mice failed to alter the pattern of cytokines produced after infection. These data show that even in the absence of IFN-gamma receptors, T helper cell (Th) 1-type responses still develop in genetically resistant mice with no evidence for the expansion of Th2 cells.

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Type
research article
DOI
10.1084/jem.181.3.961
Author(s)
Swihart, K.
Fruth, U.
Messmer, N.
Hug, K.
Behin, R.
Huang, S.
Del Giudice, G.
Aguet, M.  
Louis, J. A.
Date Issued

1995

Published in
Journal of Experimental Medicine
Volume

181

Issue

3

Start page

961

End page

71

Note

World Health Organization Immunology Research and Training Center, University of Lausanne, Epalinges, Switzerland.

Editorial or Peer reviewed

REVIEWED

Written at

OTHER

EPFL units
UPAGU  
Available on Infoscience
December 12, 2007
Use this identifier to reference this record
https://infoscience.epfl.ch/handle/20.500.14299/15465
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