A monoclonal antibody recognizing very late activation antigen-4 inhibits eosinophil accumulation in vivo

• Published in: The Journal of experimental medicine Vol. 177; no. 2; pp. 561 - 566
• Main Authors: WEG, V. B, WILLIAMS, T. J, LOBB, R. R, NOURSHARGH, S
• Format: Journal Article
• Language: English
• Published: New York, NY Rockefeller University Press 01-02-1993; The Rockefeller University Press
• Subjects: Animals; Antibodies, Monoclonal - immunology; Biological and medical sciences; Edema - immunology; Eosinophils - immunology; Fundamental and applied biological sciences. Psychology; Guinea Pigs; Inflammation; Inflammation - immunology; Leukotriene B4 - pharmacology; Molecular and cellular biology; Passive Cutaneous Anaphylaxis; Platelet Activating Factor - pharmacology; Receptors, Very Late Antigen - immunology; Zymosan - pharmacology; Immunomodulation; Rodentia; Chemical mediator; Inflammation; Monoclonal antibody; Eosinophil; Mechanism; Binding protein; In vivo; Vertebrata; Mammalia; Guinea pig; Integrin; Infiltration
• ISSN: 0022-1007; 1540-9538
• DOI: 10.1084/jem.177.2.561

Using an in vivo test system, the role of the beta 1 integrin very late activation antigen-4 (VLA-4) in eosinophil accumulation in allergic and nonallergic inflammatory reactions was investigated. Eosinophil infiltration and edema formation were measured as the local accumulation of intravenously injected 111In-labeled eosinophils and 125I-human serum albumin. The inflammatory reactions investigated were a passive cutaneous anaphylaxis (PCA) reaction and responses elicited by intradermal soluble inflammatory mediators (platelet-activating factor, leukotriene B4, C5a des Arg), arachidonic acid, and zymosan particles. The in vitro pretreatment of 111In-eosinophils with the anti-VLA-4 monoclonal antibody (mAb) HP1/2, which crossreacts with guinea pig eosinophils, suppressed eosinophil accumulation in all the inflammatory reactions investigated. Eosinophil accumulation was inhibited to the same extent when mAb HP1/2 was administered intravenously. It is interesting that HP1/2 had no effect on stimulated edema formation. These results suggest a role for VLA-4 in eosinophil accumulation in vivo and indicate a dissociation between the inflammatory events of eosinophil accumulation and edema formation.