Expression of intercellular adhesion molecule‐1 (ICAM‐1) in nasal epithelial cells of atopic subjects: a mechanism for increased rhinovirus infection? - Bianco, A.; Whiteman, S. C.; Sethi, S. K.; Allen, J. T.; Knight, R. A.; Spiteri, M. A. (Clinical and experimental immunology, 2000)
Keywords: Adult; Allergens - immunology; Allergic diseases; Asthma - etiology; Asthma - metabolism; Asthma - virology; Biological and medical sciences; Cells, Cultured - metabolism; Cells, Cultured - virology; Disease Susceptibility; Epithelial Cells - metabolism; Epithelial Cells - virology; Female; Human rhinovirus 14; Humans; Hypersensitivity, Immediate - complications; Hypersensitivity, Immediate - metabolism; Hypersensitivity, Immediate - virology; Immunity to Infection; Immunopathology; intercellular adhesion molecule 1; Intercellular Adhesion Molecule-1 - biosynthesis; Intercellular Adhesion Molecule-1 - genetics; intercellular adhesion molecule‐1 HRV infection atopy nasal polyps; Male; Medical sciences; Nasal Mucosa - metabolism; Nasal Mucosa - virology; Nasal Polyps - metabolism; Nasal Polyps - pathology; Nasal Polyps - virology; Picornaviridae Infections - etiology; Picornaviridae Infections - virology; Poaceae; Pollen - immunology; Receptors, Virus - biosynthesis; Receptors, Virus - genetics; Respiratory and ent allergic diseases; Rhinitis, Allergic, Seasonal - complications; Rhinovirus - isolation & purification; Rhinovirus - physiology; Seasons; Up-Regulation; Human; Immunopathology; Allergy; Nose disease; Pathophysiology; Intercellular adhesion molecule 1; Respiratory disease; Picornaviridae; Cell adhesion molecule; Asthma; Virus; Infection; Nose; ENT disease; Epithelial cell; Obstructive pulmonary disease; Benign neoplasm; Polyp; Rhinovirus