List of Titles

Mis-expression of GATA6 re-programs cell fate during early hematopoiesis

Authors: Audiger, Cindy , Laâbi, Yacine , Nie, Junil , Gibson, Leonie , Wilson-Annan, Julie , Brook-Carter, Phillip , Kueh, Andrew , Harris, Alan , Naik, Shalin , Nutt, Stephen , Strasser, Andreas , Adams, Jerry , Bouillet, Philippe , Chopin, Michaël
Date: 2024
Type: Text , Journal article
Relation: Cell Reports Vol. 43, no. 5 (2024), p.
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Description: The traditional view of hematopoiesis is that myeloid cells derive from a common myeloid progenitor (CMP), whereas all lymphoid cell populations, including B, T, and natural killer (NK) cells and possibly plasmacytoid dendritic cells (pDCs), arise from a common lymphoid progenitor (CLP). In Max41 transgenic mice, nearly all B cells seem to be diverted into the granulocyte lineage. Here, we show that these mice have an excess of myeloid progenitors, but their CLP compartment is ablated, and they have few pDCs. Nevertheless, T cell and NK cell development proceeds relatively normally. These hematopoietic abnormalities result from aberrant expression of Gata6 due to serendipitous insertion of the transgene enhancer (E

Authors: Gray, Daniel , Kupresanin, Fiona , Berzins, Stuart , Herold, Marco , O'Reilly, Lorraine , Bouillet, Philippe , Strasser, Andreas
Date: 2012
Type: Text , Journal article
Relation: Immunity Vol. 37, no. 3 (September 2012), p. 451-462
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Description: Although the proapoptotic BH3-only protein, Bim, is required for deletion of autoreactive thymocytes, Bim-deficient mice do not succumb to extensive organ-specific autoimmune disease. To determine whether other BH3-only proteins safeguard tolerance in the absence of Bim, we screened mice lacking Bim as well as other BH3-only proteins. Most strains showed no additional defects; however, mice deficient for both Puma and Bim spontaneously developed autoimmunity in multiple organs, and their T cells could transfer organ-specific autoimmunity. Puma- and Bim-double-deficient mice had a striking accumulation of mature, single-positive thymocytes, suggesting an additional defect in thymic deletion was the basis for disease. Transgenic mouse models of thymocyte deletion by peripheral neoantigens confirmed that the loss of Bim and Puma allowed increased numbers of autoreactive thymocytes to escape deletion. Our data show that Puma cooperates with Bim to impose a thymic-deletion checkpoint to peripheral self-antigens and cement the notion that defects in apoptosis alone are sufficient to cause autoimmune disease.
Description: C1

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