Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
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Enzyme
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Query: UMLS:C0001511 (
Adhesion
)
5,955
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Interleukin 5 (IL-5) is a T-cell derived cytokine that induces eosinophil growth and differentiation in both mouse and human bone marrow cultures. Elevated levels of IL-5 as well as eosinophils have been detected in the sputum and Bronchoalveolar lavage (BAL) fluids of asthmatics. Since the recruitment of inflammatory cells to tissues requires the participation of adhesion molecules, we have developed a rapid and sensitive assay to examine the effect of IL-5 and other activation stimuli on eosinophil adhesion to recombinant intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1). Human recombinant IL-5, granulocyte-macrophage colony stimulating factor (GM-CSF), interleukin 3 (IL-3), tumour necrosis factor alpha (TNF-alpha), RANTES, MCP-3, C5a, PAF, fMLP, PMA and ConA all induced adhesion of purified eosinophils obtained from normal donors to ICAM-1 and VCAM-1 in a dose and time dependent manner.
Adhesion
was rapid, within 15 minutes of culture at 37 degrees C, and plateaued within 30 minutes. Activated eosinophils also adhered rapidly to immobilized IgG via the type II Fc gamma receptor (
CD32
). Analysis of the effect of IL-5 on surface molecule expression by FACS analysis revealed increased expression of CD11b molecules and decreased expression of L-selectin, but no change in the expression of CD11a, CD18, CD29, CD49d and
CD32
. We also show that Mac-i plays an important role in the regulation of eosinophil activation, since antibodies to CD11b can block IL-5 induced adhesion to IgG and IL-5 induced degranulation.
...
PMID:A rapid activation assay for human eosinophils based on adhesion to immobilized ICAM-1, VCAM-1 and IgG. 883 40
We investigated capture and activation of flowing human neutrophils through their Fc-receptors, FcRgammaIIIB (CD16) and FcRgammaIIA (
CD32
). Immobilised platelets bearing murine monoclonal antibody against glycoprotein IIbIIIA were able to capture and activate flowing neutrophils. The activation response was inhibited by antibody blockade of neutrophil
CD32
. However, capture only occurred efficiently at wall shear stress below 0.1 Pa if platelet P-selectin was blocked. If neutrophils were perfused over immobilised human IgG, many adhered at 0.025 or 0.05 Pa, but not at 0.1 Pa.
Adhesion
was reduced by blockade of CD16 or
CD32
, but blockade of CD16 had the greater effect. When neutrophils were perfused over a combination of purified P-selectin and IgG, blockade of CD16 and
CD32
inhibited activation of captured cells. Immunoglobulin deposited in tissue could capture and activate slow-flowing neutrophils. It might also potentiate inflammatory responses at higher stress if presented along with selectins. The dominant FcR for capture of neutrophils was CD16, but with murine antibody,
CD32
played a greater role.
...
PMID:Capture of flowing human neutrophils by immobilised immunoglobulin: roles of Fc-receptors CD16 and CD32. 1693 43