T Follicular Helper Cell-Germinal Center B Cell Interaction Strength Regulates Entry into Plasma Cell or Recycling Germinal Center Cell Fate

Publication date: 17 April 2018
Source:Immunity, Volume 48, Issue 4
Author(s): Wataru Ise, Kentaro Fujii, Katsuyuki Shiroguchi, Ayako Ito, Kohei Kometani, Kiyoshi Takeda, Eiryo Kawakami, Kazuo Yamashita, Kazuhiro Suzuki, Takaharu Okada, Tomohiro Kurosaki
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^loCD69^hi expressing a transcription factor IRF4 and higher-affinity B cell receptors (BCRs) or Bcl6^hiCD69^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^loCD69^hi cell formation. Furthermore, we found that expression of intercellular adhesion molecule 1 (ICAM-1) and signaling lymphocytic activation molecule (SLAM) in Bcl6^loCD69^hi cells was higher than in Bcl6^hiCD69^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.

Graphical abstract

Teaser

Ise et al. identify the plasma cell-prone LZ GC B cells whose generation relies on the amount of CD40 signal. Higher expression of ICAM-1 and SLAM in those cells facilitates more stable contacts with Tfh cells, suggesting that strength of Tfh-GC B cell interaction critically regulates formation of plasma cell precursors.


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