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The Regulation of Immunity to Leishmania Major

The Regulation of Immunity to Leishmania Major Experimental infection with the intracellular protozoan Leishmania major con­ stitutes a particularly versatile model for assessing the role of CD4+ subset de­ velopment in the host response to infectious disease. The association of Th l development with control of infection, and of Th2 cell development with pro­ gressive disease, has been well established. The capacity to manipulate the out­ come, using distinct immunologic interventions, in both genetically resistant and susceptible mice has identified key effector cytokines that must be present during the time of initial priming of T cells in order to affect the CD4 switch phenotype. Roles for interferon-y (IFN-y), interleukin 12 (IL-12), and IL-4 in T h l and Th2 maturation have been demonstrated, although additional undefined signals are required. Study of the genetically susceptible BALB/c mouse has shown fail­ ure to downmodulate IL-4 production in response to infection, a response that is critically associated with the failure to develop appropriate Thl responses. Use of the murine L. major model continues to elucidate new methods for vaccine development and suggests a promising system for identification of genes that determine susceptibility to inf ection. INTRODUCTION Infection of inbred strains of mice with Leishmania major comprises an ex­ http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Immunology Annual Reviews

The Regulation of Immunity to Leishmania Major

Annual Review of Immunology , Volume 13 (1) – Apr 1, 1995

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Publisher
Annual Reviews
Copyright
Copyright 1995 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0732-0582
eISSN
1545-3278
DOI
10.1146/annurev.iy.13.040195.001055
pmid
7612219
Publisher site
See Article on Publisher Site

Abstract

Experimental infection with the intracellular protozoan Leishmania major con­ stitutes a particularly versatile model for assessing the role of CD4+ subset de­ velopment in the host response to infectious disease. The association of Th l development with control of infection, and of Th2 cell development with pro­ gressive disease, has been well established. The capacity to manipulate the out­ come, using distinct immunologic interventions, in both genetically resistant and susceptible mice has identified key effector cytokines that must be present during the time of initial priming of T cells in order to affect the CD4 switch phenotype. Roles for interferon-y (IFN-y), interleukin 12 (IL-12), and IL-4 in T h l and Th2 maturation have been demonstrated, although additional undefined signals are required. Study of the genetically susceptible BALB/c mouse has shown fail­ ure to downmodulate IL-4 production in response to infection, a response that is critically associated with the failure to develop appropriate Thl responses. Use of the murine L. major model continues to elucidate new methods for vaccine development and suggests a promising system for identification of genes that determine susceptibility to inf ection. INTRODUCTION Infection of inbred strains of mice with Leishmania major comprises an ex­

Journal

Annual Review of ImmunologyAnnual Reviews

Published: Apr 1, 1995

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