| First Author | Yang Z | Year | 2012 |
| Journal | Immunity | Volume | 36 |
| Issue | 5 | Pages | 857-72 |
| PubMed ID | 22406270 | Mgi Jnum | J:187336 |
| Mgi Id | MGI:5436208 | Doi | 10.1016/j.immuni.2012.02.009 |
| Citation | Yang Z, et al. (2012) Fluorescent in vivo detection reveals that IgE(+) B cells are restrained by an intrinsic cell fate predisposition. Immunity 36(5):857-72 |
| abstractText | IgE antibodies may be protective in parasite immunity, but their aberrant production can lead to allergic disease and life-threatening anaphylaxis. Despite the importance of IgE regulation, few studies have directly examined the B cells that express IgE, because these cells are rare and difficult to detect. Here, we describe fluorescent IgE reporter mice and validate a flow cytometry procedure to allow sensitive and specific identification of IgE-expressing B cells in vivo. Similar to IgG1(+) cells, IgE(+) B cells differentiated into germinal center (GC) B cells and plasma cells (PCs) during primary immune responses to a T cell-dependent hapten-protein conjugate and the helminth Nippostrongylus brasiliensis. However, the participation of IgE(+) B cells in GCs was transient. IgE(+) B cells had an atypical propensity to upregulate the transcription factor Blimp-1 and undergo PC differentiation. Most IgE(+) PCs were short lived and showed reduced affinity maturation, revealing intrinsic mechanisms that restrict the IgE antibody response. |
