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.
Male
0301 basic medicine
Mice, Inbred BALB C
Antibodies, Monoclonal
Leishmaniasis, Cutaneous
Th1 Cells
Interleukin-12
Animals; Antibodies, Monoclonal/immunology; Female; Interferon-gamma/physiology; Interleukin-12/physiology; Interleukin-4/physiology; Leishmania major; Leishmaniasis, Cutaneous/genetics; Leishmaniasis, Cutaneous/immunology; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Receptors, Interferon/physiology; Th1 Cells/immunology
3. Good health
Mice, Inbred C57BL
Interferon-gamma
Mice
03 medical and health sciences
Animals
Female
Interleukin-4
Leishmania major
Receptors, Interferon
DOI:
10.1084/jem.181.3.961
Publication Date:
2004-06-24T07:56:10Z
AUTHORS (9)
ABSTRACT
Mice with homologous disruption of the gene coding for ligand-binding chain interferon (IFN) gamma receptor and derived from a strain genetically resistant to infection Leishmania major have been used study further role this cytokine in differentiation functional CD4+ T cell subsets vivo resistance infection. Wild-type 129/Sv/Ev mice are parasite, developing only small lesions, which resolve spontaneously within 6 wk. In contrast, lacking IFN-gamma develop large, progressing lesions. After infection, lymph nodes (LN) spleens both wild-type knockout showed an expansion cells producing as revealed by measuring supernatants specifically stimulated cells, enumerating IFN-gamma-producing Northern blot analysis transcripts. No biologically active interleukin (IL) 4 was detected vitro-stimulated LN or spleen infected deficient mice. Reverse transcription polymerase reaction primers specific IL-4 similar message levels types The observed were comparable those found similarly C57BL/6 significantly lower than BALB/c Anti-IFN-gamma treatment failed alter pattern cytokines produced after These data show that even absence receptors, helper (Th) 1-type responses still no evidence Th2 cells.
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