Linked Life Data

9759905

Source:http://linkedlifedata.com/resource/pubmed/id/9759905

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1998-10-22
pubmed:abstractText
Therapeutic preparations of normal human IgG for i.v. use (i.v.Ig) exhibit a broad spectrum of immunoregulatory activities in vitro and in vivo. I.v.Ig has been shown to inhibit the proliferation of activated B and T lymphocytes and of several autonomously growing cell lines. In this study, we demonstrate that i.v.Ig induces apoptosis in leukemic cells of lymphocyte and monocyte lineage and in CD40-activated normal tonsillar B cells, involving, at least in part, Fas (CD95/APO-1) and activation of caspases. I.v.Ig-induced apoptosis was higher in Fas-sensitive HuT78 cells than in Fas-resistant HuT78.B1 mutant cells, and soluble Fas inhibited IVIg-induced apoptosis. I.v.Ig immunoprecipitated Fas from Fas-expressing transfectants and recognized purified Fas/glutathione-S-transferase fusion proteins upon immunoblotting. Affinity-purified anti-Fas Abs from i.v.Ig induced apoptosis of CEM T cells at a 120-fold lower concentration than unfractionated i.v.Ig. Inhibitors of cysteine proteases of the caspase family, caspase 1 (IL-1beta-converting enzyme) and caspase 3 (Yama/CPP32b), partially inhibited i.v.Ig-induced apoptosis of CEM cells. Furthermore, cleavage of poly(A)DP-ribose polymerase into an 85-kDa signature death fragment was observed in CEM cells following i.v.Ig treatment. Thus, normal IgG induces apoptosis in lymphocytes and monocytes. Our results provide evidence for a role of Fas, bring new insights into the mechanisms of action of i.v.Ig in autoimmune diseases, and suggest a role of normal Ig in controlling cell death and proliferation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
161
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3781-90
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:9759905-Animals, pubmed-meshheading:9759905-Antibody Specificity, pubmed-meshheading:9759905-Antigens, CD40, pubmed-meshheading:9759905-Antigens, CD95, pubmed-meshheading:9759905-Apoptosis, pubmed-meshheading:9759905-B-Lymphocytes, pubmed-meshheading:9759905-Cell Death, pubmed-meshheading:9759905-Cell Division, pubmed-meshheading:9759905-Cell Line, pubmed-meshheading:9759905-Cysteine Endopeptidases, pubmed-meshheading:9759905-Enzyme Activation, pubmed-meshheading:9759905-Humans, pubmed-meshheading:9759905-Immune Sera, pubmed-meshheading:9759905-Immunoglobulins, Intravenous, pubmed-meshheading:9759905-Lymphocyte Activation, pubmed-meshheading:9759905-Mice, pubmed-meshheading:9759905-Mice, Inbred MRL lpr, pubmed-meshheading:9759905-Monocytes, pubmed-meshheading:9759905-Palatine Tonsil, pubmed-meshheading:9759905-T-Lymphocytes, pubmed-meshheading:9759905-Tumor Cells, Cultured
pubmed:year
1998
pubmed:articleTitle
Therapeutic preparations of normal polyspecific IgG (IVIg) induce apoptosis in human lymphocytes and monocytes: a novel mechanism of action of IVIg involving the Fas apoptotic pathway.
pubmed:affiliation
Institut National de la Santé et de la Recherche Médicale U430, Université Pierre et Marie Curie, Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't