期刊
IMMUNITY
卷 48, 期 4, 页码 702-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2018.03.027
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资金
- Ministry of Education, Culture, Sports, Science and Technology in Japan [17K08883, 26221306, 21229007]
- Japan Science Technology Agency [CREST J098501018, JST/PRESTO JPMJPR15F3]
- SENSHIN Medical Research Foundation
- Grants-in-Aid for Scientific Research [21229007, 16KT0196, 26221306, 17K08883] Funding Source: KAKEN
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.
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