| First Author | Pivniouk VI | Year | 1999 |
| Journal | J Clin Invest | Volume | 103 |
| Issue | 12 | Pages | 1737-43 |
| PubMed ID | 10377180 | Mgi Jnum | J:119608 |
| Mgi Id | MGI:3702837 | Citation | Pivniouk VI, et al. (1999) SLP-76 deficiency impairs signaling via the high-affinity IgE receptor in mast cells. J Clin Invest 103(12):1737-43 |
| abstractText | SLP-76 is an adapter protein expressed in T cells and myeloid cells that is a substrate for ZAP-70 and Syk. SLP-76-deficient mice exhibit a profound block in T-cell development. We found that although SLP-76 is expressed in mouse mast cells, SLP-76(-/-) mice have normal numbers of mast cells in their skin and bronchi. SLP-76(-/-) mice are resistant to IgE-mediated passive anaphylaxis. SLP-76(-/-) mice sensitized with IgE anti-dinitrophenyl (DNP) and then challenged with DNP-HSA developed only mild and transient tachycardia, failed to increase their plasma histamine level, and all survived the antigen challenge. Bone marrow-derived mast cells (BMMCs) from SLP76(-/-) mice failed to release beta-hexosaminidase and to secrete IL-6 after FcepsilonRI cross-linking. Tyrosine phosphorylation of phospholipase C-gamma1 (but not of Syk) and calcium mobilization in response to IgE cross-linking were reduced in SLP-76-deficient BMMCs. These results suggest that SLP-76 plays an important role in FcepsilonRI-mediated signaling in mast cells. |
