| First Author | Gross B | Year | 2002 |
| Journal | Eur J Immunol | Volume | 32 |
| Issue | 4 | Pages | 1121-8 |
| PubMed ID | 11920580 | Mgi Jnum | J:115527 |
| Mgi Id | MGI:3691895 | Doi | 10.1002/1521-4141(200204)32:4<1121::AID-IMMU1121>3.0.CO;2-R |
| Citation | Gross B, et al. (2002) SWAP-70-deficient mast cells are impaired in development and IgE-mediated degranulation. Eur J Immunol 32(4):1121-8 |
| abstractText | Cross-linking of the high-affinity IgE receptor (FcepsilonRI) on mast cell activates signaling pathways that trigger degranulation and the release of multiple pro-inflammatory mediators. Mature,immature and precursor mast cells are degranulation competent. We show here that the signaling protein SWAP-70 has a function in mast cell biology. While not found in many cell types, we find that apart from B cells, mast cells also express SWAP-70. In activated B cells, SWAP-70 shuttles between cytoplasm and nucleus, but in mast cells it is confined to the cytoplasm. SWAP-70(ko/ko) (double knockout) mice have reduced numbers of mature mast cells, and these are degranulation competent. However, although immature mast cells from SWAP-70(ko/ko) mice respond normally to SCF and IL-3 and have functional granules, their FcepsilonRI-mediated degranulation is inhibited. Thus, in mast cells SWAP-70 plays a role both in establishing the initial competence to degranulate and to develop into mature mast cells. |
