Serum levels of tetranectin, intercellular adhesion molecule-1 and interleukin-10 in B-chronic lymphocytic leukemia

1999 ◽  
Vol 32 (8) ◽  
pp. 639-645 ◽  
Author(s):  
Elli F Kamper ◽  
Anastasios D PapahilisS ◽  
Maria K Angelopoulou ◽  
Ludmila T Kopeikina ◽  
Marina P Siakantaris ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Adhesion Molecule ◽  
Serum Levels ◽  
Interleukin 10 ◽  
Intercellular Adhesion ◽  
Lymphocytic Leukemia ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

scholarly journals Serum levels of soluble intercellular adhesion molecule 1 are increased in chronic B-lymphocytic leukemia and correlate with clinical stage and prognostic markers [see comments]

Blood ◽  
1994 ◽  
Vol 84 (9) ◽  
pp. 3010-3016 ◽  
Author(s):  
I Christiansen ◽  
C Gidlof ◽  
AC Wallgren ◽  
B Simonsson ◽  
TH Totterman
Keyword(s):  
Adhesion Molecule ◽  
Doubling Time ◽  
Clinical Stage ◽  
Serum Levels ◽  
Serum Markers ◽  
Intercellular Adhesion ◽  
Lymphocytic Leukemia ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Soluble Intercellular Adhesion Molecule

The serum levels of soluble intercellular adhesion molecule 1 (ICAM-1) were significantly elevated (P < .001) in patients with chronic B- lymphocytic leukemia (B-CLL, n = 113) compared with healthy controls (n = 31). sICAM-1 levels in B-CLL were positively correlated to the tumor mass as reflected by the modified Rai and the Binet staging systems, lymphocyte counts, and isolated spleno/hepatomegaly. During disease progression or regression on cytoreductive therapy, the circulating sICAM-1 levels changed accordingly. sICAM-1 was also correlated to a kinetic parameter such as the lymphocyte doubling time. Furthermore, the serum sICAM-1 levels were inversely correlated to hemoglobin levels in patients with early clinical stage, and this may turn out to be of prognostic value. sICAM-1 was compared with other serum markers said to reflect disease activity in B-CLL, ie, soluble CD23, thymidine kinase, lactate dehydrogenase (LDH), and beta 2-microglobulin. sICAM-1 was equally well or better correlated to clinical stage and lymphocyte doubling time. In univariate regression analysis, all serum markers but LDH correlated with survival, and in multivariate analysis, sICAM-1 was the only marker approaching significance for additional prognostic information when included after clinical stage and lymphocyte doubling time. Based on the present observations, it appears that prospective studies repeatedly monitoring serum sICAM-1 in B-CLL are justified.

scholarly journals Serum levels of soluble intercellular adhesion molecule 1 are increased in chronic B-lymphocytic leukemia and correlate with clinical stage and prognostic markers [see comments]

Blood ◽  
1994 ◽  
Vol 84 (9) ◽  
pp. 3010-3016 ◽  
Author(s):  
I Christiansen ◽  
C Gidlof ◽  
AC Wallgren ◽  
B Simonsson ◽  
TH Totterman
Keyword(s):  
Adhesion Molecule ◽  
Doubling Time ◽  
Clinical Stage ◽  
Serum Levels ◽  
Serum Markers ◽  
Intercellular Adhesion ◽  
Lymphocytic Leukemia ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Soluble Intercellular Adhesion Molecule

Abstract The serum levels of soluble intercellular adhesion molecule 1 (ICAM-1) were significantly elevated (P < .001) in patients with chronic B- lymphocytic leukemia (B-CLL, n = 113) compared with healthy controls (n = 31). sICAM-1 levels in B-CLL were positively correlated to the tumor mass as reflected by the modified Rai and the Binet staging systems, lymphocyte counts, and isolated spleno/hepatomegaly. During disease progression or regression on cytoreductive therapy, the circulating sICAM-1 levels changed accordingly. sICAM-1 was also correlated to a kinetic parameter such as the lymphocyte doubling time. Furthermore, the serum sICAM-1 levels were inversely correlated to hemoglobin levels in patients with early clinical stage, and this may turn out to be of prognostic value. sICAM-1 was compared with other serum markers said to reflect disease activity in B-CLL, ie, soluble CD23, thymidine kinase, lactate dehydrogenase (LDH), and beta 2-microglobulin. sICAM-1 was equally well or better correlated to clinical stage and lymphocyte doubling time. In univariate regression analysis, all serum markers but LDH correlated with survival, and in multivariate analysis, sICAM-1 was the only marker approaching significance for additional prognostic information when included after clinical stage and lymphocyte doubling time. Based on the present observations, it appears that prospective studies repeatedly monitoring serum sICAM-1 in B-CLL are justified.

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.

Soluble Intercellular Adhesion Molecule-1 (sICAM-1) in serum and cerebrospinal fluid of demyelinating diseases of the central and peripheral nervous system

1998 ◽  
Vol 4 (1) ◽  
pp. 39-44 ◽  
Author(s):  
M Trojano ◽  
C Avolio ◽  
M Ruggieri ◽  
F De Robertis ◽  
F Giuliani ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Adhesion Molecule ◽  
Serum Levels ◽  
Intercellular Adhesion ◽  
Demyelinating Diseases ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Mean Values ◽  
Soluble Intercellular Adhesion Molecule

Serum and cerebrospinal fluid (CSF) soluble Intercellular adhesion molecule-1 (ICAM-1) levels were evaluated (ELISA) in 22 untreated and 13 corticosteroid-treated active relapsing remitting (RR) Multiple Sclerosis (MS), in 10 untreated and 10 corticosteroid-treated Guillain-Barré syndrome (GBS) and in 17 non-inflammatory neurological diseases (NIND). Twenty-eight clinically inactive RR MS were assayed for serum sICAM-1 before and after 3 months treatment of 8 MIU rIFNb-1b taken s.c. every other day. High sICAM-1 serum levels above the NIND values were found in untreated clinically active MS and in untreated GBS (P50.05) but not in the untreated clinically inactive MS group. The active MS group showed significantly (P=0.0001) higher sICAM-1 serum levels if compared to the inactive group. Corticosteroid-treated active MS and GBS patients showed lower (P50.05) serum sICAM-1 levels than the corresponding untreated groups. Serum sICAM-1 levels after 3 months of rIFNb-1b treatment (P50.0001, paired t-test) resulted increased compared to pretreatment values in MS. The mean values of CSF/serum sICAM-1: CSF/serum Albumin ratios (sICAM-1 Index) in active untreated MS patients were higher compared to NIND (P50.005) and to corticosteroid-treated MS group (P=0.01). sICAM Index values in GBS did not differ from those in NIND. The results seem to suggest potential roles for serum sICAM-1 in downregulating the ongoing inflammatory response at the blood-brain barrier level and for CSF sICAM-1 in the maintenance of a central nervous system local immune response.

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