Human memory T cells express intercellular adhesion molecule-1 which can be increased by interleukin 2 and interferon-γ

1990 ◽  
Vol 20 (2) ◽  
pp. 337-341 ◽  
Author(s):  
Anne-Marie Buckle ◽  
Nancy Hogg
Keyword(s):  
T Cells ◽  
Adhesion Molecule ◽  
Memory T Cells ◽  
Interleukin 2 ◽  
Human Memory ◽  
Interferon Γ ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

scholarly journals Interleukin-10 Inhibits Interferon-γ–Induced Intercellular Adhesion Molecule-1 Gene Transcription in Human Monocytes

Blood ◽  
1997 ◽  
Vol 89 (12) ◽  
pp. 4461-4469 ◽  
Author(s):  
Seng Song ◽  
Hsiang Ling-Hu ◽  
Kenneth A. Roebuck ◽  
Mohammed F. Rabbi ◽  
Raymond P. Donnelly ◽  
...  
Keyword(s):  
Tyrosine Phosphorylation ◽  
Gene Transcription ◽  
Adhesion Molecule ◽  
Interleukin 10 ◽  
Interferon Γ ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Human Monocytes ◽  
Intercellular Adhesion Molecule 1 ◽  
Ifn Γ

Abstract Interleukin-10 (IL-10) is a potent monocyte regulatory cytokine that inhibits gene expression of proinflammatory mediators. In this study, we investigated the mechanism by which IL-10 downregulates expression of intercellular adhesion molecule-1 (ICAM-1) on the cell surface of normal human monocytes activated with interferon-γ (IFN-γ). IL-10 inhibition of IFN-γ–induced ICAM-1 expression was apparent as early as 3 hours and was blocked by an anti–IL-10 antibody but not by an isotype-matched control antibody. Northern blot analysis showed that IL-10 reduced the accumulation of ICAM-1 mRNA in IFN-γ–stimulated monocytes. IL-10 inhibition of ICAM-1 steady-state mRNA was detected at 3 hours and remained at 24 hours. Nuclear run-on transcription assays showed that IL-10 inhibited the rate of IFN-γ–induced transcription of the ICAM-1 gene, and mRNA stability studies showed that IL-10 did not alter the half-life of IFN-γ–induced ICAM-1 message. Thus, IL-10 inhibits IFN-γ–induced ICAM-1 expression in monocytes primarily at the level of gene transcription. Activation of IFN-γ–responsive genes requires tyrosine phosphorylation of the transcriptional factor STAT-1α (signal transducer and activator of transcription-1α). However, IL-10 did not affect IFN-γ–induced tyrosine phosphorylation of STAT-1α or alter STAT-1α binding to the IFN-γ response element (IRE) in the ICAM-1 promoter. Instead, IL-10 prevented IFN-γ–induced binding activity at the NF-κB site of the tumor necrosis factor α (TNF-α)–responsive NF-κB/C-EBP composite element in the ICAM-1 promoter. These data indicate that IL-10 inhibits IFN-γ–induced transcription of the ICAM-1 gene by a regulatory mechanism that may involve NF-κB.

scholarly journals Lymphocytic Infiltration and Expression of Intercellular Adhesion Molecule-1 in Photochemically Induced Ischemia of the Rat Cortex

1995 ◽  
Vol 15 (1) ◽  
pp. 42-51 ◽  
Author(s):  
Sebastian Jander ◽  
Matthias Kraemer ◽  
Michael Schroeter ◽  
Otto W. Witte ◽  
Guido Stoll
Keyword(s):  
T Cells ◽  
Adhesion Molecule ◽  
Immune Reaction ◽  
Lymphocytic Infiltration ◽  
Intercellular Adhesion ◽  
Border Zone ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Ischemic Lesion ◽  
New Approach

The contribution of the immune system to the pathogenesis of ischemic lesions is still uncertain. We have analyzed leukocyte infiltration in photochemically induced focal ischemia of the rat parietal cortex by immunocytochemistry. Between 1 and 2 days after photothrombosis, CD5 + T cells adhered to subpial and cortical vessels and infiltrated the ischemic lesion prior to macrophages. By day 3 numerous T cells and some macrophages, whose number increased further between day 3 and day 7, had infiltrated the border zone around the lesion sparing the center. In addition, CD5–/CD8+ lymphocytes that probably represent natural killer cells were found. Intercellular adhesion molecule-1 (ICAM-1) was expressed on endothelial cells on days 1 and 2 and in the border zone on infiltrating leukocytes from day 3 to day 7. Starting on day 7, macrophages infiltrated the core of the lesion to remove debris. When the entire lesion was covered by macrophages at day 14, the number of T cells had decreased and ICAM-1 immunoreactivity was no longer found in or around the infarct. In conclusion, our study shows that ischemic lesions can lead to a local immune reaction in the CNS. Thus, blocking of lymphocyte-derived cytokines or cell adhesionmolecules may provide a new approach to confining the sequelae of stroke.

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