Overexpression of BCL2 cooperates with Myd88/Cd79b/Prdm1 to induce massive expansion of aberrant spontaneous splenic GCBs. (A) Immunohistochemistry of unimmunized spleens from 8-week-old mice that were Aicda^cre/+ and control, Rosa26^{LSLBCL2-IRES-GFP} (BCL2), Myd88/Cd79b/Prdm1, Myd88/Cd79b/BCL2, or Myd88/Cd79b/Prm1/BCL2. Sections were stained for IgD and GL7, CD138, Ephrin-B1, or CD35. Scale bar = 500 μm. Additional examples of Aicda^cre/+ Myd88/Cd79b/BCL2 or Aicda^cre/+ Myd88/Cd79b/Prdm1/BCL2 mice are shown in supplemental Figure 3A. (B) High-power images of areas marked in panel A. Sections were stained for IgD and GL7, CD35, or CD4. Red asterisks mark areas of GL7⁺ cell infiltration into T-cell areas of spleens of Myd88/Cd79b/Prdm1/BCL2 animals. Scale bar = 100 μm. (C) Flow cytometry of splenocytes from Aicda^cre/+ Myd88/Cd79b/BCL2 or Aicda^cre/+ Myd88/Cd79b/Prdm1/BCL2 mice. (D) Expression of Ephrin-B1, CXCR4, or CCR6 on splenic GCs or MBCs from Aicda^cre/+ Myd88/Cd79b/Prdm1/BCL2 mice. (E) Expression of LZ or DZ GC markers on splenic GCBs from Aicda^cre/+ control or Myd88/Cd79b/Prdm1/BCL2 mice. (F) Frequency of splenic GCBs, MBCs, or PBs/PCs in 8- to 10-week-old Aicda^cre/+ control, Myd88/Cd79b/Prdm1, Myd88/Cd79b/BCL2, or Myd88/Cd79b/Prdm1/BCL2. Data in panels A and B are representative of 2 to 5 mice per genotype; data in panels C to E are from one experiment representative of 4 independent experiments with 1 mouse per group; and data in panel F are pooled from 8 independent experiments with up to 1 mouse per group per experiment. **P < .01, ***P < .001, ****P < .0001, unpaired two-tailed t test.