| First Author | Kaku H | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 3 | Pages | 1667-74 |
| PubMed ID | 19592656 | Mgi Jnum | J:151598 |
| Mgi Id | MGI:4354479 | Doi | 10.4049/jimmunol.0900056 |
| Citation | Kaku H, et al. (2009) Fas apoptosis inhibitory molecule enhances CD40 signaling in B cells and augments the plasma cell compartment. J Immunol 183(3):1667-74 |
| abstractText | Fas apoptosis inhibitory molecule (FAIM) was cloned as a mediator of Fas resistance that is highly evolutionarily conserved but contains no known effector motifs. In this study, we report entirely new functions of FAIM that regulate B cell signaling and differentiation. FAIM acts to specifically enhance CD40 signaling for NF-kappaB activation, IRF-4 expression, and BCL-6 down-regulation in vitro, but has no effect on its own or in conjunction with LPS or anti-Ig stimulation. In keeping with its effects on IRF-4 and BCL-6, FAIM overexpression augments the plasma cell compartment in vivo. These results indicate that FAIM is a new player on the field of B cell differentiation and acts as a force multiplier for a series of events that begins with CD40 engagement and ends with plasma cell differentiation. |
