Liquan Xue1, Stephan W Morris1, 2, 4, Carlos Orihuela3, Elaine Tuomanen3, Xiaoli Cui1, Renren Wen5
& Demin Wang5, 6, 71
Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
2
Department of Hematology/Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
3
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
4
Department of Pediatrics, University of Tennessee, College of Medicine, Memphis, Tennessee 38163, USA.
5
Blood Research Institute, The Blood Center of Southeastern Wisconsin, Milwaukee, Wisconsin 53226, USA.
6
Model Animal Research Center, Nanjing University, Nanjing, China.
7
Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Correspondence should be addressed to Stephan W Morris steve.morris@stjude.org or Demin Wang dwang@bcsew.edu
B activation after lymphocyte antigen receptor stimulation. Using knockout mice, we show that absence of Bcl10 impeded conversion from transitional type 2 to mature follicular B cells and caused substantial decreases in marginal zone and B1 B cells. Bcl10-deficient B cells showed no excessive apoptosis. However, both Bcl10-deficient follicular and marginal zone B cells failed to proliferate normally, although Bcl10-deficient marginal zone B cells uniquely failed to activate NF-
