| First Author | Wang N | Year | 2006 |
| Journal | Am J Respir Cell Mol Biol | Volume | 35 |
| Issue | 2 | Pages | 206-10 |
| PubMed ID | 16528012 | Mgi Jnum | J:144137 |
| Mgi Id | MGI:3830159 | Doi | 10.1165/rcmb.2005-0294OC |
| Citation | Wang N, et al. (2006) The costimulatory molecule SLAM is critical for pulmonary allergic responses. Am J Respir Cell Mol Biol 35(2):206-10 |
| abstractText | 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. |
