Journal article
Proapoptotic BIM impacts B lymphoid homeostasis by limiting the survival of mature B cells in a cell-autonomous manner
R Liu, A King, P Bouillet, DM Tarlinton, A Strasser, J Heierhorst
Frontiers in Immunology | FRONTIERS MEDIA SA | Published : 2018
Abstract
The proapoptotic BH3-only protein BIM (Bcl2l11) plays key roles in the maintenance of multiple hematopoietic cell types. In mice, germline knockout or conditional pan-hematopoietic deletion of Bim results in marked splenomegaly and significantly increased numbers of B cells. However, it has remained unclear whether these abnormalities reflect the loss of cell-intrinsic functions of BIM within the B lymphoid lineage and, if so, which stages in the lifecycle of B cells are most impacted by the loss of BIM. Here, we show that B lymphoid-specific conditional deletion of Bim during early development (i.e., in pro-B cells using Mb1-Cre) or during the final differentiation steps (i.e., in transitio..
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Awarded by State Government of Victoria
Funding Acknowledgements
This work was supported by a NHMRC Senior Research Fellowship (1022469), a Worldwide Cancer Research grant (16-0156), grants-in-aid from the 5-point Foundation and the Margaret Walkom Bequest to JH; an Australian Postgraduate Award to AK; NHMRC Senior Principal Research Fellowship (1020363), NHMRC program grant (1016701), Cancer Council Victoria grant (1052309), Leukemia and Lymphoma Society (LLS) SCOR grant (7001-13) to AS; NHMRC program grant (1054925) and NHMRC Principal Research Fellowship (1060675) to DT; and NHMRC Independent Research Institutes Infrastructure Support, and Victorian State Government Operational Infrastructure Support grants.