       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).

