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57
Direct Visualization of Antigen-specific CD8 � T Cells during the Primary Immune Response to Epstein-Barr Virus In Vivo
"... Primary infection with virus can stimulate a vigorous cytotoxic T cell response. The magnitude of the antigen-specific component versus the bystander component of a primary T cell response remains controversial. In this study, we have used tetrameric major histocompatibility complex–peptide complexe ..."
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Primary infection with virus can stimulate a vigorous cytotoxic T cell response. The magnitude of the antigen-specific component versus the bystander component of a primary T cell response remains controversial. In this study, we have used tetrameric major histocompatibility complex–peptide complexes to directly visualize antigen-specific cluster of differentration (CD)8 � T cells during the primary immune response to Epstein-Barr virus (EBV) infection in humans. We show that massive expansion of activated, antigen-specific T cells occurs during the primary response to this virus. In one individual, T cells specific for a single EBV epitope comprised 44 % of the total CD8 � T cells within peripheral blood. The majority of the antigen-specific cells had an activated/memory phenotype, with expression of human histocompatibility leukocyte antigen (HLA) DR, CD38, and CD45RO, downregulation of CD62 leukocyte (CD62L), and low levels of expression of CD45RA. After recovery from AIM, the frequency of antigen-specific T cells fell in most donors studied, although populations of antigen-specific cells continued to be easily detectable for at least 3 yr. Primary infection with virus can stimulate a vigorous T cell response, with activation and proliferation of lymphocytes
Differential expression of Fas (CD95) and Fas ligand on normal human phagocytes: implications for the regulation of apoptosis in neutrophils
, 1996
"... Human neutrophils, monocytes, and eosinophils are known to undergo apoptotic cell death. The Fas/Fas ligand pathway has been implicated as an important cellular pathway mediating apoptosis in diverse cell types. We conducted studies to examine the importance of the Fas/ FasL system in normal human p ..."
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Cited by 44 (5 self)
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Human neutrophils, monocytes, and eosinophils are known to undergo apoptotic cell death. The Fas/Fas ligand pathway has been implicated as an important cellular pathway mediating apoptosis in diverse cell types. We conducted studies to examine the importance of the Fas/ FasL system in normal human phagocytes. Although Fas expression was detected on neutrophils, monocytes, and eosinophils, constitutive expression of FasL was restricted to neutrophils. The three types of phagocytes demonstrated differential sensitivity to Fas-induced apoptosis. Only neutrophils were highly susceptible to rapid apoptosis in vitro after stimulation with activating anti-Fas IgM (mAb CH-11). Fas-mediated neutrophil apoptosis was suppressed by incubation with G-CSF, GM-CSF, 1FN-',/, TNF-0~, or dexamethasone, as well as the selective tyrosine kinase inhibitors, herbimycin A and genistein. Spontaneous neutrophil death in vitro was partially suppressed by Fas-Ig fusion protein or antagonistic anti-Fas IgGi (mAb ZB4). In coculture experiments, neutrophils released a soluble factor inducing death in Fas-susceptible Jurkat cells via a mechanism sensitive to the presence of Fas-Ig or anti-Fas IgG 1. Immunoblot analysis using specific anti-human FasL IgG ~ (mAb No. 33) identified a 37-kD protein in lysates of freshly isolated neutrophils and a 30-kD protein in the culture supematant of neutrophils
Perforin, a cytotoxic molecule which mediates cell necrosis, is not required for the early control of mycobacterial infection in mice. Infect. Immun
, 1997
"... Perforin, a cytotoxic molecule which mediates cell necrosis, is not required for the early ..."
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Cited by 37 (4 self)
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Perforin, a cytotoxic molecule which mediates cell necrosis, is not required for the early
The relative role of lymphocyte granule exocytosis versus death receptor-mediated cytotoxicity in viral pathophysiology
- J
, 1998
"... This article cites 120 articles, 59 of which can be accessed free at: ..."
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Cited by 11 (2 self)
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This article cites 120 articles, 59 of which can be accessed free at:
Haussinger D. Regulation of CD95 (APO-1/Fas) receptor and ligand expression by lipopolysaccharide and dexamethasone in parenchymal and nonparenchymal rat liver cells. HEPATOLOGY
"... The effect of lipopolysaccharide (LPS) on the expression of CD95 (APO-1/Fas) receptor and ligand (CD95L) was studied in primary cultures of rat liver Kupffer cells (KCs), sinusoidal endothelial cells (SECs), and parenchymal cells (PCs) at the messenger RNA (mRNA) level and by means of immunocytochem ..."
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Cited by 10 (3 self)
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The effect of lipopolysaccharide (LPS) on the expression of CD95 (APO-1/Fas) receptor and ligand (CD95L) was studied in primary cultures of rat liver Kupffer cells (KCs), sinusoidal endothelial cells (SECs), and parenchymal cells (PCs) at the messenger RNA (mRNA) level and by means of immunocytochemistry. LPS treatment of KCs and SECs led to a three- to five-fold increase in CD95L mRNA levels within 6 hours, which declined thereafter. Within 24 hours, the number of KCs and SECs staining positive for CD95L strongly increased. After a lag phase of 12 hours after LPS addition, in both cell types the mRNA levels for the soluble CD95 isoform increased approximately 10-fold; however, the number of KCs and SECs staining positive for transmembrane CD95 remained low and did not significantly increase. Compared with nonparenchymal cells, CD95L mRNA levels in primary hepatocyte cultures were low in the absence and presence of LPS. On the other hand, functionally active CD95 expression markedly increased in response to LPS in these cells. Dexamethasone diminished the LPS-induced stimulation of CD95L expression in nonparenchymal cells but markedly stimulated CD95L expression in PCs. Apoptosis of PCs and thymic lymphocytes was stimulated by the addition of supernatants derived from LPS-treated KC or SEC cultures and was apparently mediated by CD95L as assessed by its sensitivity to inhibitors of the CD95-dependent apoptotic pathway in PCs. The data suggest a complex and timely coordinated interplay between the various liver cell populations with respect to LPS-induced activation of the apoptotic machinery with potential relevance for immunoregulation. (HEPATOLOGY
IL-6 is increased in the cerebellum of autistic brain and alters neural cell adhesion, migration and synaptic formation.
- J Neuroinflamm
, 2011
"... Abstract Background: Although the cellular mechanisms responsible for the pathogenesis of autism are not understood, a growing number of studies have suggested that localized inflammation of the central nervous system (CNS) may contribute to the development of autism. Recent evidence shows that IL- ..."
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Abstract Background: Although the cellular mechanisms responsible for the pathogenesis of autism are not understood, a growing number of studies have suggested that localized inflammation of the central nervous system (CNS) may contribute to the development of autism. Recent evidence shows that IL-6 has a crucial role in the development and plasticity of CNS. Methods: Immunohistochemistry studies were employed to detect the IL-6 expression in the cerebellum of study subjects. In vitro adenoviral gene delivery approach was used to over-express IL-6 in cultured cerebellar granule cells. Cell adhesion and migration assays, DiI labeling, TO-PRO-3 staining and immunofluorescence were used to examine cell adhesion and migration, dendritic spine morphology, cell apoptosis and synaptic protein expression respectively.
Characterisation of glycosylphosphatidylinositol-linked molecule CD55/Decayaccelerating factor as the receptor for antibody SC-1-induced apoptosis, Cancer Res. 59
, 1999
"... This article cites 45 articles, 14 of which you can access for free at: ..."
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Cited by 5 (2 self)
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This article cites 45 articles, 14 of which you can access for free at:
Characterization of novel nuclear targeting and apoptosis-inducing domains in FAS associated factor 1
, 1998
"... FAS associated factor 1 (FAF1) has been described as an unusual protein that binds to the intracellular portion of the apoptosis signal transducing receptor FAS/Apo-1 and potentiates apoptosis in L-cells. By means of mRNA differential display we have identified the avian homologue (qFAF) as a fibrob ..."
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FAS associated factor 1 (FAF1) has been described as an unusual protein that binds to the intracellular portion of the apoptosis signal transducing receptor FAS/Apo-1 and potentiates apoptosis in L-cells. By means of mRNA differential display we have identified the avian homologue (qFAF) as a fibroblast growth factor-inducible gene in pluripotent cells from E0 quail embryos during mesoderm induction in vitro. Later during embryonic development, qFAF expression is ubiquitous. We confirm that qFAF is associated with FAS, and show that it is phosphorylated on serine residues and localized to the nucleus. By in vitro mutagenesis we have delimited a novel nuclear targeting domain to a short 35 amino acid alpha-helical region in the amino-terminal half of the protein. The nuclear function of qFAF remains unclear. However, a probably dominant negative deletion mutant of qFAF causes apoptosis of transfected cells. This function resides in the carboxyterminal domain of qFAF which shares remarkable sequence homologies with a putative ubiquitin conjugating enzyme from Caenorhabditis elegans. Our data indicate a complex function for FAF, which may be executed during FAS signalling and/or in the ubiquitination pathway, and may be essential for cell differentiation and survival.
Characterization of the non-functional Fas ligand of gld mice
- Int
, 1995
"... Mice homozygous for either the gld or Ipr mutation develop autoimmune diseases and progressive lymphadenopathy. The Ipr mutation Is characterized by the absence of functional Fas, whereas gld mice exhibit an Inactive FasL due to a point mutation proximal to the extracellular C-terminus. The structur ..."
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Mice homozygous for either the gld or Ipr mutation develop autoimmune diseases and progressive lymphadenopathy. The Ipr mutation Is characterized by the absence of functional Fas, whereas gld mice exhibit an Inactive FasL due to a point mutation proximal to the extracellular C-terminus. The structural repercussions of this amino acid substitution remain unknown. Here we report that FasL is expressed at similar levels on the surface of activated T lymphocytes from gld and wild-type mice. Using a polyclonal anti-FasL antibody, indistinguishable amounts of a 40 kDa protein are detected In both gld and wild-type splenocytes. The molecular model of FasL, based on the known structure of TNF-a, predicts that the Phe->Leu gld mutation is located at the protomer interface which is close to the FasR interaction site. We conclude that the gld mutation allows normal FasL biosynthesis, surface expression and oligomerlzatlon, but Induces structural alterations to the Fas binding region leading to the phenotyplc changes observed.
B Cells Directly Tolerize CD8 � T Cells
"... This report investigates the response of CD8 � T cells to antigens presented by B cells. When C57BL/6 mice were injected with syngeneic B cells coated with the K b-restricted ovalbumin (OVA) determinant OVA 257–264, OVA-specific cytotoxic T lymphocyte (CTL) tolerance was observed. To investigate the ..."
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This report investigates the response of CD8 � T cells to antigens presented by B cells. When C57BL/6 mice were injected with syngeneic B cells coated with the K b-restricted ovalbumin (OVA) determinant OVA 257–264, OVA-specific cytotoxic T lymphocyte (CTL) tolerance was observed. To investigate the mechanism of tolerance induction, in vitro–activated CD8 � T cells from the K b-restricted, OVA-specific T cell receptor transgenic line OT-I (OT-I cells) were cultured for 15 h with antigen-bearing B cells, and their survival was determined. Antigen recognition led to the killing of the B cells and, surprisingly, to the death of a large proportion of the OT-I CTLs. T cell death involved Fas (CD95), since OT-I cells deficient in CD95 molecules showed preferential survival after recognition of antigen on B cells. To investigate the tolerance mechanism in vivo, naive OT-I T cells were adoptively transferred into normal mice, and these mice were coinjected with antigen-bearing B cells. In this case, OT-I cells proliferated transiently and were then lost from the secondary lymphoid compartment. These data provide the first demonstration that B cells can directly tolerize CD8 � T cells, and suggest that this occurs via CD95-mediated, activation-induced deletion. Key words:
