       Document 0340
 DOCN  M9630340
 TI    Immunopathology of interleukin (IL) 2-deficient mice: thymus dependence
       and suppression by thymus-dependent cells with an intact IL-2 gene.
 DT    9603
 AU    Kramer S; Schimpl A; Hunig T; Institute for Virology and Immunobiology,
       University of; Wurzburg, Germany.
 SO    J Exp Med. 1995 Dec 1;182(6):1769-76. Unique Identifier : AIDSLINE
       MED/96096450
 AB    Interleukin (IL) 2-deficient mice develop a fatal immunopathology
       characterized by lymphoadenopathy, splenomegaly, T cell infiltration of
       the bone marrow, loss of B cells, anemia, and inflammation of the gut.
       The thymus dependence of these disease symptoms was tested by
       introducing the IL-2 mutation into athymic mice. With the exception of
       an increase in CD8+ intrahepatic alpha/beta T cells, IL-2 deficiency had
       no detectable effect on leukocyte composition or health of athymic mice,
       indicating a key role for thymus-derived T cells in the initiation of
       disease and demonstrating that B cell development and survival are
       independent of IL-2. In adoptive transfer studies, lymph node and spleen
       cells from euthymic IL-2-deficient mice induced disease in athymic mice
       with an intact IL-2 gene, suggesting that thymus-independent
       IL-2-expressing cells are unable to control the development of immune
       pathology. Both IL-2+ and IL-2-/- bone marrow cells repopulated the
       thymus and the peripheral T cell compartment of the recombination
       activator gene 2-deficient recipients, and chimeras that had received
       IL-2-deficient bone marrow developed immune pathology. Disease
       development was, however, fully or at least partially prevented when 30%
       of the bone marrow inoculum was derived from mice able to express IL-2.
       These results demonstrate that the IL-2 deficiency syndrome depends on
       the intrathymic differentiation of T cells carrying the IL-2 mutation,
       and that the abnormal activation of IL-2-deficient lymphocytes can be
       controlled by thymus-derived but not thymus-independent lymphocytes.
 DE    Animal  B-Lymphocytes/IMMUNOLOGY  Bone Marrow/PATHOLOGY  CD4-Positive
       T-Lymphocytes/*IMMUNOLOGY  CD8-Positive T-Lymphocytes/*IMMUNOLOGY
       Immunologic Deficiency Syndromes/*IMMUNOLOGY/PATHOLOGY
       Interleukin-2/DEFICIENCY/*PHYSIOLOGY  Liver/IMMUNOLOGY  Mice  Mice,
       Inbred C57BL  Mice, Mutant Strains  Mice, Nude  Plant
       Proteins/PHYSIOLOGY  Support, Non-U.S. Gov't  T-Lymphocyte
       Subsets/*IMMUNOLOGY  Thymus Gland/*PHYSIOLOGY  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

