Fig 1: BTLA Deficiency in T Cells Leads to GC B Cell Expansion in the Setting of Bcl-2 Overexpression(A) Frequency of CD45.2 splenic Fo and GC B cells of Bcl-2 transgenic origin in mixed BM chimeras reconstituted with 30%–50% Hvem+/+, Hvem+/-, or Hvem-/- Eµ-BCL2-tg CD45.2 BM and 50%–70% WT Eµ-BCL2-tg CD45.1/2 BM at day 7 after SRBC immunization. Data are pooled from three experiments.(B and C) The frequency (B) and number (C) of spontaneously forming splenic GC B cells in mice reconstituted for 6–14 weeks with Hvem+/+or Hvem-/- BM transduced with MSCV-Bcl2-Thy1.1. Data are pooled from two experiments.(D) Representative flow-cytometric analysis of spontaneous GC formation in the spleen after 8 weeks of reconstitution with Btlaf/f or Btlaf/fCd4Cre BM transduced with MSCV-Bcl2-Thy1.1. Irradiated Rag2-/- or Tcrb-/- mice were used as hosts.(E and F) The frequency (E) and number (F) of spontaneously forming splenic GC B cells in BM chimeras from (D). Data are pooled from three experiments.(G) VH- and VL-region PCR analysis of GC B cells from two Btlaf/fCd4Cre chimeras with splenic GC outgrowths > 20% and two Btlaf/f control chimeras.Unpaired two-tailed Student’s test (B,C, E, and F): *p < 0.05, **p < 0.01, ****p < 0.0001.