[PDF][PDF] T follicular helper cell-germinal center B cell interaction strength regulates entry into plasma cell or recycling germinal center cell fate

W Ise, K Fujii, K Shiroguchi, A Ito, K Kometani… - Immunity, 2018 - cell.com
W Ise, K Fujii, K Shiroguchi, A Ito, K Kometani, K Takeda, E Kawakami, K Yamashita
Immunity, 2018cell.com
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 …
Summary
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, Bcl6loCD69hi expressing a transcription factor IRF4 and higher-affinity B cell receptors (BCRs) or Bcl6hiCD69hi with lower-affinity BCRs, favored the plasma cell or recycling GC cell fate, respectively. Mechanistically, CD40 acted as a dose-dependent regulator for Bcl6loCD69hi cell formation. Furthermore, we found that expression of intercellular adhesion molecule 1 (ICAM-1) and signaling lymphocytic activation molecule (SLAM) in Bcl6loCD69hi cells was higher than in Bcl6hiCD69hi 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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