| First Author | Kataoka TR | Year | 2015 |
| Journal | Int Immunol | Volume | 27 |
| Issue | 2 | Pages | 95-103 |
| PubMed ID | 25239131 | Mgi Jnum | J:222331 |
| Mgi Id | MGI:5644372 | Doi | 10.1093/intimm/dxu087 |
| Citation | Kataoka TR, et al. (2015) CD72 negatively regulates mouse mast cell functions and down-regulates the expression of KIT and FcepsilonRIalpha. Int Immunol 27(2):95-103 |
| abstractText | CD72 is a transmembrane protein belonging to the C-type lectin family that is expressed by various hematopoietic cells. When bound to its natural ligand, CD100 (semaphorin 4D), CD72 inhibits the KIT-mediated responses of human mast cells, but not IgE/FcepsilonRI-mediated mast cell degranulation. We extended these findings to examine the role of CD72 in mouse mast cells. CD72 expression was detected in mouse bone marrow-derived mast cells (mBMMCs). As for human mast cells, an agonistic antibody against CD72 (K10.6) suppressed the KIT-mediated cell growth of, IL-6 production by and chemotaxis of mBMMCs. However, in contrast to human mast cells, the IgE-triggered degranulation of mBMMCs was suppressed by K10.6. K10.6 did not affect the phosphorylation of SHP-1 in mBMMCs, although SHP-1 mediated the inhibitory effects of CD72 in human mast cells. Administration of K10.6 induced phosphorylation of the ubiquitin ligase Cbl-b and decreased the expression of KIT and FcepsilonRIalpha on the surface of murine mast cells. We also observed expression of CD72 in a mouse neoplastic cell line, P815, harboring gain-of-function mutations in KIT genes. In addition, we found that K10.6 activated Cbl-b, down-regulated KIT expression and suppressed the mutated KIT-driven growth of these cells. Thus, the mechanism by which CD72 mediates inhibitory effects in mast cells is species-dependent. |
