Journal
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
Volume 35, Issue 2, Pages 206-210Publisher
AMER THORACIC SOC
DOI: 10.1165/rcmb.2005-0294OC
Keywords
allergic inflammation; asthma; costimulatory molecules; murine; SLAM
Funding
- NHLBI NIH HHS [HL 5672, HL 67684] Funding Source: Medline
- NIAID NIH HHS [AI 142681] Funding Source: Medline
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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 cytolkine 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 cytolkines and Th1 cytolkines were decreased in SLAM-deficient mice. These data support the concept that SLAM plays a crucial role in allergic responses.
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