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Host susceptibility factors to cutaneous leishmaniasis
D E Jones1, M M Elloso, P Scott
1Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. jonesdou@mail.med. upenn.edu
Frontiers in Bioscience : a Journal and Virtual Library
|November 20, 1998
Summary
Mouse models reveal that resistance to Leishmania infection relies on CD4+ Th1 cells and IFN-gamma, promoting macrophage activation. Susceptibility involves a Th2 response and IL-4, leading to uncontrolled parasite growth.
Area of Science:
- Immunology
- Parasitology
- Infectious Disease
Background:
- Host-pathogen interactions are crucial in disease pathogenesis.
- Leishmania infections are studied in mouse models to understand immune responses.
Purpose of the Study:
- To elucidate the immunological factors determining resistance or susceptibility to Leishmania.
- To define the roles of CD4+ T helper cell subsets in leishmaniasis.
Main Methods:
- Utilized a mouse model of Leishmania infection.
- Analyzed immune responses, focusing on T helper cell differentiation (Th1 vs. Th2) and cytokine production.
Main Results:
- Resistance is associated with CD4+ Th1 cells and Interferon-gamma (IFN-gamma), which activate macrophages to kill Leishmania.
- Susceptibility is linked to a Th2 response and Interleukin-4 (IL-4), resulting in high antibody titers but impaired macrophage function and increased parasite load.
Conclusions:
- The balance between Th1 and Th2 responses dictates the outcome of Leishmania infection.
- Mouse models are valuable for understanding in vivo T cell commitment and immune-mediated control of parasitic diseases.