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1996-02-26
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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).