| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* Department of Pharmacology, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel;
Department of Otolaryngology-Head and Neck Surgery, The Hebrew University School of Medicine, Hadassah Medical Center, Jerusalem, Israel;
Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267;
Division of Allergy and Immunology, Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45267; and
¶ David R. Bloom Center for Pharmacology, The Hebrew University of Jerusalem, Jerusalem, Israel
Eosinophils are involved in a variety of allergic, parasitic, malignant, and idiopathic disorders by releasing a variety of factors including specific granule proteins, lipid mediators, and proinflammatory and immunoregulatory cytokines and chemokines. In addition, they interact with various cell types in the inflamed tissue. Yet, the mechanism of eosinophil activation is still poorly understood. Recently, we described the expression and function of the CD2-subfamily of receptors and especially 2B4 on human eosinophils. In this study we focus on CD48, the high-affinity ligand of 2B4. CD48 is a GPI-anchored protein involved in cellular activation, costimulation, and adhesion, but has not been studied on eosinophils. We demonstrate that human eosinophils from atopic asthmatics display enhanced levels of CD48 expression and that IL-3 up-regulates CD48 expression. Furthermore, cross-linking CD48 on human eosinophils triggers release of eosinophil granule proteins. Assessment of CD48 expression in a murine model of experimental asthma revealed that CD48 is induced by allergen challenge and partially regulated by IL-3. Additionally, anti-IL-3 reduces CD48 expression and the degree of airway inflammation. Thus, CD48 is an IL-3-induced activating receptor on eosinophils, likely involved in promoting allergic inflammation.
This article has been cited by other articles:
|
|
 |
|
  C. M. Rocha-de-Souza, B. Berent-Maoz, D. Mankuta, A. E. Moses, and F. Levi-Schaffer Human Mast Cell Activation by Staphylococcus aureus: Interleukin-8 and Tumor Necrosis Factor Alpha Release and the Role of Toll-Like Receptor 2 and CD48 Molecules Infect. Immun., October 1, 2008; 76(10): 4489 - 4497. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Yoon, A. Terada, and H. Kita CD66b Regulates Adhesion and Activation of Human Eosinophils J. Immunol., December 15, 2007; 179(12): 8454 - 8462. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Munitz, I. Bachelet, F. D. Finkelman, M. E. Rothenberg, and F. Levi-Schaffer CD48 Is Critically Involved in Allergic Eosinophilic Airway Inflammation Am. J. Respir. Crit. Care Med., May 1, 2007; 175(9): 911 - 918. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
