Published ahead of print on March 9, 2006, doi:10.1165/rcmb.2005-0294OC
© 2006 American Thoracic Society DOI: 10.1165/rcmb.2005-0294OC The Costimulatory Molecule SLAM Is Critical for Pulmonary Allergic ResponsesDivision of Immunology, Beth Israel Deaconess Medical Center; and Pulmonary and Critical Care Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts Correspondence and requests for reprints should be addressed to Dr. Patricia W. Finn, Respiratory and Critical Care Division, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115. E-mail: pwfinn{at}ucsd.edu T-cell activation plays an essential role in the generation of the pulmonary inflammation that is manifest in allergic asthma. Optimal T-cell activation requires not only presentation of antigen with the major histocompatibility complex, but also concurrent signaling through costimulatory molecules. The costimulatory molecule SLAM (Signaling Lymphocytic Activation Molecule, CD150) is a glycoprotein expressed on activated lymphocytes and antigen-presenting cells. Disruption of the SLAM gene demonstrated that SLAM-induced signal transduction pathways regulate cytokine production by T helper (Th)2 cells and macrophages. Here we tested the postulate that the costimulatory molecule SLAM may be critical for allergic inflammation in a murine model. SLAM-deficient mice did not manifest allergen-induced bronchoalveolar lavage eosinophilia, increased serum IgE, or heightened airway responses compared with wild-type mice. Allergen-induced Th2 cytokines and Th1 cytokines were decreased in SLAM-deficient mice. These data support the concept that SLAM plays a crucial role in allergic responses.
Key Words: allergic inflammation • asthma • costimulatory molecules • murine • SLAM This article has been cited by other articles:
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