| First Author | Sekine Y | Year | 2014 |
| Journal | J Immunol | Volume | 192 |
| Issue | 8 | Pages | 3488-95 |
| PubMed ID | 24616480 | Mgi Jnum | J:210230 |
| Mgi Id | MGI:5569844 | Doi | 10.4049/jimmunol.1300886 |
| Citation | Sekine Y, et al. (2014) Signal-transducing adaptor protein-2 controls the IgE-mediated, mast cell-mediated anaphylactic responses. J Immunol 192(8):3488-95 |
| abstractText | Signal-transducing adaptor protein-2 (STAP-2) is a recently identified adaptor protein that regulates immune and inflammatory responses through interactions with a variety of signaling and transcriptional molecules. In the current study, we clarified the physiological role of STAP-2 in mast cell function, a key mediator of IgE-associated allergic responses. STAP-2 is constitutively expressed in mast cells. STAP-2 deficiency in mast cells greatly enhances FcepsilonRI-mediated signals, resulting in the increased tyrosine phosphorylation of the phospholipase C-gamma isoform, calcium mobilization, and degranulation. Of importance, STAP-2-deficient mice challenged with DNP-BSA after passive sensitization with anti-DNP IgE show more severe rectal temperature decrease than do wild-type mice. STAP-2-deficient mice also show increased vascular permeability and more severe cutaneous anaphylaxis after DNP-BSA injection. These regulatory functions performed by STAP-2 indicate that there is an interaction between STAP-2 and FcepsilonRI. In addition, our previous data indicate that STAP-2 binds to the phospholipase C-gamma isoform and IkappaB kinase-beta. Therefore, our data described in this article strongly suggest that manipulation of STAP-2 expression in mast cells may control the pathogenesis of allergic diseases and have the potential for treating patients with allergy. |
