| First Author | Ise W | Year | 2018 |
| Journal | Immunity | Volume | 48 |
| Issue | 4 | Pages | 702-715.e4 |
| PubMed ID | 29669250 | Mgi Jnum | J:272538 |
| Mgi Id | MGI:6284485 | Doi | 10.1016/j.immuni.2018.03.027 |
| Citation | Ise W, et al. (2018) T Follicular Helper Cell-Germinal Center B Cell Interaction Strength Regulates Entry into Plasma Cell or Recycling Germinal Center Cell Fate. Immunity 48(4):702-715.e4 |
| abstractText | Higher- or lower-affinity germinal center (GC) B cells are directed either to plasma cell or GC recycling, respectively; however, how commitment to the plasma cell fate takes place is unclear. We found that a population of light zone (LZ) GC cells, Bcl6(lo)CD69(hi) expressing a transcription factor IRF4 and higher-affinity B cell receptors (BCRs) or Bcl6(hi)CD69(hi) with lower-affinity BCRs, favored the plasma cell or recycling GC cell fate, respectively. Mechanistically, CD40 acted as a dose-dependent regulator for Bcl6(lo)CD69(hi) cell formation. Furthermore, we found that expression of intercellular adhesion molecule 1 (ICAM-1) and signaling lymphocytic activation molecule (SLAM) in Bcl6(lo)CD69(hi) cells was higher than in Bcl6(hi)CD69(hi) cells, thereby affording more stable T follicular helper (Tfh)-GC B cell contacts. These data support a model whereby commitment to the plasma cell begins in the GC and suggest that stability of Tfh-GC B cell contacts is key for plasma cell-prone GC cell formation. |
