1. High Levels of Susceptibility and T Helper 2 Response in MyD88-Deficient Mice Infected withLeishmania majorAre Interleukin-4 Dependent
- Author
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André Gessner, Martin Röllinghoff, Joachim Gläsner, and Andrea Debus
- Subjects
Myeloid ,medicine.medical_treatment ,Immunology ,Antibodies, Protozoan ,Leishmaniasis, Cutaneous ,Biology ,Microbiology ,Mice ,Th2 Cells ,Immunity ,medicine ,Animals ,Leishmania major ,Receptors, Immunologic ,Receptor ,Interleukin 4 ,Adaptor Proteins, Signal Transducing ,Mice, Knockout ,Mice, Inbred BALB C ,Th1 Cells ,biology.organism_classification ,Antigens, Differentiation ,Mice, Inbred C57BL ,Infectious Diseases ,medicine.anatomical_structure ,Cytokine ,Myeloid Differentiation Factor 88 ,Knockout mouse ,Female ,Parasitology ,Disease Susceptibility ,Interleukin-4 ,Fungal and Parasitic Infections - Abstract
Myeloid differentiation protein 88 (MyD88) is a general adaptor for the signaling cascade through receptors of the Toll/IL-1R family. When infected withLeishmania majorparasites, MyD88-deficient mice displayed a dramatically enhanced parasite burden in their tissues similar to that found in susceptible BALB/c mice. In contrast, MyD88 knockout mice did not develop ulcerating lesions despite a lack of interleukin-12 (IL-12) production and a predominant T helper 2 cell response. Blockade of IL-4 produced early (day 1) after infection restored a protective T helper 1 response in MyD88 knockout mice.
- Published
- 2003
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