|
31. |
Differential secretion of tumor necrosis factor‐α and granulocyte/macrophage colony‐stimulating factors but not interferon‐γ from CD4 compared to CD8 human T cell clones |
|
European Journal of Immunology,
Volume 19,
Issue 1,
1989,
Page 197-200
Graham Pawelec,
Kurt Schaudt,
Arnika Rehbein,
Friedrich W. Busch,
Preview
|
PDF (311KB)
|
|
摘要:
AbstractTumor necrosis factor‐alpha (TNF‐α) is a pleiotropic lymphokine which may have important regulatory effects on immune responses. It is shown here that eight alloreactive CD4 T cell clones (TCC) secreted significant amounts of TNF‐α after stimulation with either specific alloantigen or 12‐O‐tetradecanoylphorbol 13‐acetate together with the calcium ionophore ionomycin (up to 50 ng/ml/24 h/106cells) whereas CD8 TCC failed to do so (max. 2 ng/ml/24 h/106cells). The CD8 TCC also secreted markedly less granulocyte/macrophage colony‐stimulating factor than the CD4 cells. However, this was not indicative of a general decrease of lymphokine production by CD8 cells because CD4 and CD8 TCC both secreted similar amounts of interferon‐gamma. These results show that regulatory CD4 lymphocytes can produce large amounts of TNF‐α, whereas CD8 effecto
ISSN:0014-2980
DOI:10.1002/eji.1830190132
出版商:WILEY‐VCH Verlag GmbH
年代:1989
数据来源: WILEY
|
32. |
Expression of the p75 interleukin 2‐binding protein on CD34‐8‐Tac‐cells from autoimmune MRL/MP‐lpr/lprmice |
|
European Journal of Immunology,
Volume 19,
Issue 1,
1989,
Page 201-204
José C. gutierrez‐Ramos,
Luis Pezzi,
Ronald Palacios,
Carlos Martínez‐A.,
Preview
|
PDF (458KB)
|
|
摘要:
AbstractThe recently described (Sharon, M. et al.,Science1986.234: 859) interleukin 2 (IL 2)‐binding molecule p75 was detected in the CD34‐8‐Tac‐“double‐negative” cell population selectively expanded in lupus‐like autoimmune mice MRL/MP‐lpr/lprusing cross‐linking studies. Scatchard analysis of the IL2 binding revealed the existence of approximately 4700 sites per cell with an apparent Kdof 1500 pM. The cell line LD1.T3B, derived from this population, shared surface markers and the p75 presence/p55 absence of IL 2‐binding proteins with itsin vivocounterpart, displaying around 3100 sites per cell with a Kdof about 1300 pM. Functional studies showed that high doses of IL 2 had an inhibitory effect on the autonomous growth of this cell line in the absence of the development of killer activity. This study provides evidence of the functional abilities of p75, and shows that the use of Tac/p55 surface expression only to evaluate IL 2 receptors and T cell activation can be an oversimplification
ISSN:0014-2980
DOI:10.1002/eji.1830190133
出版商:WILEY‐VCH Verlag GmbH
年代:1989
数据来源: WILEY
|
33. |
The expression of I‐A correlates with the uptake of interferon‐γ by macrophages |
|
European Journal of Immunology,
Volume 19,
Issue 1,
1989,
Page 205-208
Antonio Celada,
Richard A. Maki,
Preview
|
PDF (452KB)
|
|
摘要:
AbstractThe current studies were designed to examine some of the requirements for I‐A expression when macrophages (MΨ) were treated with interferon‐gamma (IFN‐γ). In order to define the minimum time required for IFN‐γ to induce surface expression of I‐A antigen on bone marrow‐derived MΨ, cells were incubated with IFN‐γ for varying lengths of time, washed and thereafter incubated for 72 h before assaying I‐A surface expression. Using saturating amounts of IFN‐γ (300 IRU/ml), we found that between 0 and 30 min of IFN‐γ treatment there is a direct correlation between the length of treatment and the level of I‐A surface expression. When the steady state level of RNA for the I‐Aβgene was assayed, a low level of I‐AβRNA was seen in cells treated for 10 min with saturting amounts of IFN‐γ (300 IRU/ml) while a 30‐min or 60‐min exposure of cells to the same concentration of IFN‐γ resulted in a steady increase in the level of I‐AβRNA. Similar results were found when we measured the levels of RNA for the tumor necrosis factor and C3 complement genes, both of which are induced by IFN‐γ in MΨ. MΨ treated with low amounts of IFN‐γ (3 IRU/ml) for 30 min do not express cell surface I‐A. Cells incubated continuously for 72 h with 3 IRU/ml of IFN‐γ expressed a level of I‐A on the surface equivalent to the level of I‐A expressed on cells treated for only 30 min with 300 IRU/ml of IFN‐γ. Based on the observed correlation between either the IFN‐γ concentration or the length of time the cells were exposed to IFN‐γ, or the level of I‐A expression on MΨ
ISSN:0014-2980
DOI:10.1002/eji.1830190134
出版商:WILEY‐VCH Verlag GmbH
年代:1989
数据来源: WILEY
|
34. |
Interleukin 1 and tumor necrosis factor‐α additively increase the levels of granulocyte‐macrophage and granulocyte colony‐stimulating factor (CSF) mRNA in human fibroblasts |
|
European Journal of Immunology,
Volume 19,
Issue 1,
1989,
Page 209-212
Walter Seelentag,
Jean‐Jacques Mermod,
Pierre Vassalli,
Preview
|
PDF (629KB)
|
|
摘要:
AbstractRecombinant interleukin (IL) 1 β and tumor necrosis factor/cachectin (TNF‐α) induce, usually within 2 h, a dose‐dependent increase in the levels of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) and G‐CSF mRNA in cultured human fibroblasts. Maximal induction is reached at about 4–8 h and usually last for at least 48 h. IL 1β and TNF have additive effects on the levels of GM‐ and G‐CSF mRNA, and on the secretion of G‐CSF activity into the culture medium. IL 1α has the same additive effect that IL 1β has with TNF, but no additive effect with IL 1β. In contrast, the high basic level of M‐CSF (CSF‐1) mRNA shows little or lower variations in response to IL 1, TNF‐α or both IL 1 and TNF‐α also induce, with similar kinetics, an increase in IL 1β but not mRNA level. In contrast to what is observed with macrophages and endothelial cells,E. colilipopolysaccharide does not modify the fibroblast
ISSN:0014-2980
DOI:10.1002/eji.1830190135
出版商:WILEY‐VCH Verlag GmbH
年代:1989
数据来源: WILEY
|
35. |
Human T cell clones with specificity for insulinoma cell antigens |
|
European Journal of Immunology,
Volume 19,
Issue 1,
1989,
Page 213-216
Els Van Vliet,
Bart O. Roep,
Lex Meulenbroek,
G. Jan Bruining,
René R. P. De Vries,
Preview
|
PDF (442KB)
|
|
摘要:
AbstractSeveral lines of evidence suggest that islet‐specific T cells are important in the pathogenesis of the insulitis resulting in insulin‐dependent diabetes mellitus (IDDM). Therefore, we decided to analyze islet‐specific T cell reactivity in the peripheral blood of IDDM patients. With the use of insulinoma membranes as antigen, T cell lines were generated from peripheral blood mononuclear cells of patients with recent onset of the disease. In a proliferation assay such T cell lines responded to insulinoma membranes and, though to a lesser extent, also to fibroblast membranes, the control antigen used. One of the T cell lines was cloned. Eight clones were isolated that respond to insulinoma antigens. Five of these eight clones appeared to be specific for insulinoma membranes,i.e.they demonstrated proliferation in response to insulinoma but not fibroblast membranes. These insulinoma‐specific proliferative responses are HLA‐DR r
ISSN:0014-2980
DOI:10.1002/eji.1830190136
出版商:WILEY‐VCH Verlag GmbH
年代:1989
数据来源: WILEY
|
36. |
Absence of homologous restriction factor does not affect CTL‐mediated cytolysis |
|
European Journal of Immunology,
Volume 19,
Issue 1,
1989,
Page 217-219
Olivier P. Krähenbühl,
Hans H. Peter,
JÜRg Tschopp,
Preview
|
PDF (312KB)
|
|
摘要:
AbstractHomologous restriction factor (HRF) is a membrane protein of erythrocytes and leukocytes that inhibits the complement (C5b‐9)‐mediated lysis in a species‐restricting manner. HRF has also been reported to inhibit perforin‐mediated cytolysis and postulated to play a role in cytotoxic T lymphocyte (CTL) self‐protection. We show that paroxysmal nocturnal hemoglobinuria (PNH) erythrocytes, lacking HRF, are no more sensitive to Ca2+‐dependent human CTL‐mediated lysis than normal erythrocytes. Furthermore, mouse and normal human erythrocytes, as well as PNH erythrocytes, are similarly lysed by isolated murine perforin‐containing granules. We conclude that HRF does not inhibit perforin‐mediated lysis and therefore is not likely to play a role in CT
ISSN:0014-2980
DOI:10.1002/eji.1830190137
出版商:WILEY‐VCH Verlag GmbH
年代:1989
数据来源: WILEY
|
37. |
Masthead |
|
European Journal of Immunology,
Volume 19,
Issue 1,
1989,
Page -
Preview
|
PDF (70KB)
|
|
ISSN:0014-2980
DOI:10.1002/eji.1830190101
出版商:WILEY‐VCH Verlag GmbH
年代:1989
数据来源: WILEY
|
|