|
Asthma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Actions on ICAM1 provide a mechanism for the locus to confer susceptibility to HRV-induced asthma.
|
30339462 |
2019 |
|
Asthma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Peripheral blood from adults with COPD (n=17), asthma (n=20), and healthy participants (n=19) was examined for expression of CD16, CD62L, CD11b, CD11c, and CD54, and analyzed by flow cytometry.
|
31814717 |
2019 |
|
Asthma
|
0.600 |
Biomarker
|
disease |
CTD_human |
Both ICAM1 and ETS, and interactions between these two factors are likely to be involved in the development of asthma in childhood.
|
25003170 |
2014 |
|
Asthma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
ICAM1 gene expression was positively associated with exhaled levels of soluble ICAM1 (p = 0.04) which in turn was positively associated with asthma development (p = 0.01).
|
24393359 |
2014 |
|
Asthma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Both ICAM1 and ETS, and interactions between these two factors are likely to be involved in the development of asthma in childhood.
|
25003170 |
2014 |
|
Asthma
|
0.600 |
Biomarker
|
disease |
RGD |
Anti-inflammatory, immunomodulatory, and heme oxygenase-1 inhibitory activities of ravan napas, a formulation of uighur traditional medicine, in a rat model of allergic asthma.
|
20953388 |
2011 |
|
Asthma
|
0.600 |
Biomarker
|
disease |
CTD_human |
We utilized mice lacking ICAM-1 expression (ICAM-1(-/-)) to investigate the role of ICAM-1 in airway inflammation and AHR in TDI-induced asthma.
|
17014439 |
2006 |
|
Asthma
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
The following polymorphisms in ICAM1 were genotyped on 352 children with asthma and 270 controls: rs5491 (resulting in the amino-acid exchange K56M), rs5493 (G241S), rs5498 (rs5498" genes_norm="3383">K469E), rs5030400 (rs5030400" genes_norm="3383">R478W) and rs885743 in the 3'-untranslated region.
|
16625213 |
2006 |
|
Asthma
|
0.600 |
GeneticVariation
|
disease |
LHGDN |
The following polymorphisms in ICAM1 were genotyped on 352 children with asthma and 270 controls: rs5491 (resulting in the amino-acid exchange K56M), rs5493 (G241S), rs5498 (K469E), rs5030400 (R478W) and rs885743 in the 3'-untranslated region.
|
16625213 |
2006 |
|
Asthma
|
0.600 |
GeneticVariation
|
disease |
LHGDN |
Intercellular adhesion molecule-1 and childhood asthma.
|
16021473 |
2005 |
|
Asthma
|
0.600 |
Biomarker
|
disease |
LHGDN |
Targeting leukocyte integrins in human diseases.
|
15548573 |
2005 |
|
Asthma
|
0.600 |
Biomarker
|
disease |
LHGDN |
[Exploration of the levels and significance of serum s C5b-9, s VCAM-1, s ICZM-1 in children wit asthma].
|
15059493 |
2004 |
|
Asthma
|
0.600 |
Biomarker
|
disease |
BEFREE |
These two phenotypes can be segregated by their dependence on the ICAM-1 gene and so depend on distinct controls that appear critical for the development of lifelong airway diseases such as asthma.
|
12122108 |
2002 |
|
Asthma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Intercellular adhesion molecule 1 (ICAM-1) has a central role in airway inflammation in asthma, and it is the receptor for 90% of rhinoviruses.
|
11496238 |
2001 |
|
Asthma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Collectively, these observations provide new evidence demonstrating that activation of the CAM counterreceptor ligands ICAM-1 and LFA-1, both of which are endogenously expressed in ASM cells, elicits autologously upregulated IL-5 release and associated changes in ICAM-1 expression and agonist responsiveness in atopic asthmatic sensitized ASM.
|
10835320 |
2000 |
|
Asthma
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
ICAM-1 expression was significantly increased in bronchial epithelial cells from untreated asthmatics, but ICAM-1 was not expressed in those from steroid-dependent asthmatic patients.
|
9731032 |
1998 |
|
Asthma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Since we found that mite allergens can induce ICAM-1 on ECs, even during clinical latency, allergy may be considered as a primary event leading to asthma (through rhinovirus infection) and non-specific hyperreactivity.
|
7613226 |
1995 |
|
Asthma
|
0.600 |
Biomarker
|
disease |
BEFREE |
Up-regulation of endothelial cell adhesion molecules, specifically E-selectin and ICAM-1, is responsible for the leucocyte recruitment of the late-phase asthmatic response, while recruitment of T cells and their subsequent activation contribute to the ongoing inflammatory response of asthma.
|
7542080 |
1995 |