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1996-02-27
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Document 0480
DOCN M9630480
TI The accumulation of B220+ CD4- CD8- (DN) T cells in C3H-lpr/lpr mice is
not accelerated by the stimulation of CD8+ T cells or B220+ DN T cells
with staphylococcal enterotoxin B and occurs independently of V beta 8+
T cells.
DT 9603
AU Giese T; Davidson WF; Laboratory of Genetics, National Cancer Institute,
Bethesda, MD; 20892, USA.
SO Int Immunol. 1995 Aug;7(8):1213-23. Unique Identifier : AIDSLINE
MED/96022643
AB Mice homozygous for lpr or gld develop lymphoproliferative disease
characterized by the progressive accumulation of functionally impaired
B220+ double-negative (DN) T cells and primed CD4+ and CD8+ T cells. The
mechanisms leading to the accumulation of these T cells subsets are
poorly understood but are clearly dependent on lack of expression of Fas
in lpr mice and expression of defective FasL in gld mice. A role for V
beta 8+ T cells also has been reported. Recently, a variety of
experimental approaches revealed that the majority of B220+ DN T cells
are derived from MHC class I-selected CD8+ precursors. Here we used the
potent mitogen, staphylococcal enterotoxin B (SEB): (i) to examine the
effects of defective Fas-FasL expression on the deletion of peripheral V
beta 8+ T cells in 6- to 8- and 20-week old C3H-lpr and -gld mice, (ii)
to determine the immunocompetence of B220+ DN T cells in vivo, and (iii)
to determine if activated V beta 8+ CD8+ T cells can differentiate into
B220+ DN T cells. The role of V beta 8+ T cells in the accumulation of
B220+ DN T cells also was reinvestigated. These studies showed that
deletion pathways independent of Fas-FasL expression function in young
lpr and gld mice and delete CD4+ T cells more efficiently than CD8+ T
cells. As the mice age, these alternative pathways become less effective
and this may explain the progressive accumulation of memory T cells. No
abnormalities in tolerance induction were observed in young or diseased
mice. Stimulation of +/+, lpr and gld V beta 8+ CD8+ T cells induced the
expression of B220. B220 levels were maximal 2 days after SEB and were
undetectable 5 days later, suggesting that B220 is a transiently
expressed activation marker on CD8+ T cells. Neither the B220+ V beta 8+
CD8+ T cells nor other V beta 8+ T cell populations converted with
detectable frequency into B220+ DN T cells after single or multiple
doses of SEB. B220+ DN T cells, which are functionally anergic in vitro,
did not proliferate or undergo deletion after SEB stimulation indicating
that these cells also are functionally impaired in vivo. In contrast to
previous reports, chronic elimination of V beta 8+ T cells had no effect
on the accumulation of B220+ DN T cells.(ABSTRACT TRUNCATED AT 400
WORDS)
DE Animal Antibodies, Monoclonal/PHARMACOLOGY Antigens, CD4/IMMUNOLOGY
Antigens, CD45/*IMMUNOLOGY/METABOLISM Antigens, CD8/IMMUNOLOGY
Antigens, CD95/METABOLISM Clonal Anergy Clonal Deletion/IMMUNOLOGY
CD4-Positive T-Lymphocytes/IMMUNOLOGY CD8-Positive
T-Lymphocytes/*IMMUNOLOGY Dose-Response Relationship, Immunologic
Enterotoxins/ADMINISTRATION & DOSAGE/*IMMUNOLOGY Injections,
Intraperitoneal Interphase/IMMUNOLOGY Lymphocyte Transformation
Lymphoproliferative Disorders/PREVENTION & CONTROL Mice Mice, Inbred
C3H Mice, Mutant Strains Receptors, Antigen, T-Cell,
alpha-beta/*IMMUNOLOGY Staphylococcus aureus/*IMMUNOLOGY T-Lymphocyte
Subsets/CYTOLOGY/*IMMUNOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).