The costimulatory molecule SLAM is critical for pulmonary allergic responses.

Division of Immunology, Reth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
American Journal of Respiratory Cell and Molecular Biology (Impact Factor: 4.11). 09/2006; 35(2):206-10. DOI: 10.1165/rcmb.2005-0294OC
Source: PubMed

ABSTRACT 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.


Available from: Cox Terhorst, Aug 08, 2014
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