Mice from a genetically resistant background lacking the interferon γ receptor are susceptible to infection with Leishmania major but mount a polarized T helper cell 1-type CD4+ T cell response
Autor: | K. Swihart, G. Del Giudice, Michel Aguet, K. Hug, N. Messmer, Reza Behin, U. Fruth, Sui Huang, Jacques A. Louis |
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Rok vydání: | 1995 |
Předmět: |
Male
medicine.medical_treatment T cell Immunology Leishmaniasis Cutaneous Biology Animals Antibodies Monoclonal/immunology Female Interferon-gamma/physiology Interleukin-12/physiology Interleukin-4/physiology Leishmania major Leishmaniasis Cutaneous/genetics Leishmaniasis Cutaneous/immunology Mice Mice Inbred BALB C Mice Inbred C57BL Receptors Interferon/physiology Th1 Cells/immunology Interferon-gamma Interferon Interferon-gamma receptor medicine Immunology and Allergy Interferon gamma Interleukin 4 Receptors Interferon Antibodies Monoclonal Articles T helper cell Th1 Cells Interleukin-12 Virology Molecular biology Cytokine medicine.anatomical_structure Interleukin 12 Interleukin-4 medicine.drug |
Zdroj: | The Journal of Experimental Medicine Journal of Experimental Medicine, vol. 181, no. 3, pp. 961-971 |
ISSN: | 1540-9538 0022-1007 |
DOI: | 10.1084/jem.181.3.961 |
Popis: | 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. |
Databáze: | OpenAIRE |
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