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1996-02-27
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Document 0511
DOCN M9630511
TI Down-regulation of T-cell proliferation in response to soluble anti-CD3
antibodies through development of redirected cytolytic activity
eliminating costimulatory cells.
DT 9603
AU Lwin T; Nakashima I; Nagase F; Department of Immunology, Nagoya
University School of Medicine,; Aichi, Japan.
SO Microbiol Immunol. 1995;39(8):599-606. Unique Identifier : AIDSLINE
MED/96064269
AB CD4+ T-depleted spleen cells (CD8+ T cells) activated by anti-CD3
antibodies (aCD3) suppressed proliferation of CD8+ T-depleted spleen
cells (CD4+ T cells) and fresh normal T cells in response to aCD3.
Antigen-nonspecific cytolytic activity was induced in splenic CD8+ T
cells by stimulation with aCD3 and showed the peak level on day 3,
whereas cytolytic activity induced in CD4+ T cells was weak. Intact Ig
but not F(ab')2 of aCD3 induced and mediated cytolytic activity.
Correspondingly the cytolytic activity induced by aCD3 was directed
against target cells bearing Ig-binding Fc-receptor activity and
cytolysis was inhibited by the addition of free Ig into the assay
system. We showed that aCD3-activated T cells carried a high level of
aCD3 on their surface at the time after the peak proliferation when they
attained high cytolytic activity. This raised the possibility that the
anti-CD3-induced aCD3-redirected cytolytic activity eliminated
Fc-receptor-bearing costimulatory cells in the culture for
down-regulation of the T-cell proliferation. This view was supported by
partial restoration of anti-CD3-induced low responsiveness of CD8+ T
cells by the addition of fresh costimulatory cells. These results
suggested a new pathway of down-regulation of T-cell proliferation by
aCD3-activated cytolytic CD8+ T cells.
DE Animal Antibodies/IMMUNOLOGY Antigens, CD3/*IMMUNOLOGY Cell
Division/DRUG EFFECTS Cells, Cultured Cytotoxicity, Immunologic
CD8-Positive T-Lymphocytes/IMMUNOLOGY Down-Regulation (Physiology)
Mice Mice, Inbred BALB C T-Lymphocytes/*IMMUNOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).