Document 0643
 DOCN  M9620643
 TI    CD8+ type 1 CD44hi CD45 RBlo T lymphocytes control intracellular
       Brucella abortus infection as demonstrated in major histocompatibility
       complex class I- and class II-deficient mice.
 DT    9602
 AU    Oliveira SC; Splitter GA; Department of Animal Health and Biomedical
       Sciences, University; of Wisconsin, Madison 53706, USA.
 SO    Eur J Immunol. 1995 Sep;25(9):2551-7. Unique Identifier : AIDSLINE
       MED/96011866
 AB    Genetically engineered mice with a targeted disruption in the beta
       2-microglobulin (beta 2-m) gene or the H2-I-A beta chain (A beta) which
       lack functional CD8+ or CD4+ T cells, respectively, were used to assess
       the role of T cell subsets in Brucella abortus infection. Murine
       brucellosis was markedly exacerbated in beta 2-m-deficient mice (beta
       2-m-/-) compared to A beta mutant (A beta-/-) or C57BL/6 mice, strongly
       indicating that optimal resistance to B. abortus requires CD8+ T cells.
       Splenocytes from Brucella-primed beta 2-m-/-, A beta-/- and C57BL/6 mice
       exhibited a type 1 cytokine profile marked by elevated IFN-gamma mRNA
       expression and protein production, and basal levels of IL-2 and IL-4
       transcripts. B. abortus did not induce secretion of TGF-beta 1, but
       substantial IL-10 activity was detected in spleen cell supernatants from
       all mouse strains studied. CD8+ T cells from A beta-/- and C57BL/6 mice
       displayed a CD44hi CD45RBlo phenotype and a type 1 cytokine
       transcription profile featuring high levels of IFN-gamma mRNA.
       Additionally, we have shown the ability of C57BL/6 CD8+ CTL to kill
       Brucella-infected macrophages. This study illustrates the predominant
       role of MHC class I-restricted T cells in controlling B. abortus
       infection.
 DE    Animal  Antigens, CD44/IMMUNOLOGY  Antigens, CD45/IMMUNOLOGY  *Brucella
       abortus  Brucellosis/*IMMUNOLOGY  CD4-Positive T-Lymphocytes/IMMUNOLOGY
       CD8-Positive T-Lymphocytes/*IMMUNOLOGY  Histocompatibility Antigens
       Class I/GENETICS/*IMMUNOLOGY  Histocompatibility Antigens Class
       II/GENETICS/*IMMUNOLOGY  Mice  Mice, Inbred C57BL  Mice, Mutant Strains
       Spleen/*IMMUNOLOGY/MICROBIOLOGY  Support, Non-U.S. Gov't  Support, U.S.
       Gov't, Non-P.H.S.  JOURNAL ARTICLE

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