Document 0911 DOCN M95A0911 TI The regulation of immunity to Leishmania major. DT 9510 AU Reiner SL; Locksley RM; Department of Medicine, University of California, San Francisco; 94143, USA. SO Annu Rev Immunol. 1995;13:151-77. Unique Identifier : AIDSLINE MED/95336674 AB Experimental infection with the intracellular protozoan Leishmania major constitutes a particularly versatile model for assessing the role of CD4+ subset development in the host response to infectious disease. The association of Th1 development with control of infection, and of Th2 cell development with progressive disease, has been well established. The capacity to manipulate the outcome, 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-gamma (IFN-gamma), interleukin 12 (IL-12), and IL-4 in Th1 and Th2 maturation have been demonstrated, although additional undefined signals are required. Study of the genetically susceptible BALB/c mouse has shown failure to downmodulate IL-4 production in response to infection, a response that is critically associated with the failure to develop appropriate Th1 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 infection. DE Animal Antigen Presentation Cell Compartmentation/IMMUNOLOGY Cytokines/IMMUNOLOGY Disease Models, Animal Human Leishmania major/GROWTH & DEVELOPMENT/*IMMUNOLOGY Leishmaniasis, Cutaneous/IMMUNOLOGY Macrophage Activation Mice Mice, Inbred BALB C Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. Th1 Cells/IMMUNOLOGY Th2 Cells/IMMUNOLOGY JOURNAL ARTICLE REVIEW REVIEW, ACADEMIC SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).