Journal article
The BCL-2 pro-survival protein A1 is dispensable for T cell homeostasis on viral infection
S Tuzlak, RL Schenk, A Vasanthakumar, SP Preston, MD Haschka, D Zotos, A Kallies, A Strasser, A Villunger, MJ Herold
Cell Death and Differentiation | NATURE PUBLISHING GROUP | Published : 2017
DOI: 10.1038/cdd.2016.155
Abstract
The physiological role of the pro-survival BCL-2 family member A1 has been debated for a long time. Strong mRNA induction in T cells on T cell receptor (TCR)-engagement suggested a major role of A1 in the survival of activated T cells. However, the investigation of the physiological roles of A1 was complicated by the quadruplication of the A1 gene locus in mice, making A1 gene targeting very difficult. Here, we used the recently generated A1-/- mouse model to examine the role of A1 in T cell immunity. We confirmed rapid and strong induction of A1 protein in response to TCR/CD3 stimulation in CD4+ as well as CD8+ T cells. Surprisingly, on infection with the acute influenza HKx31 or the lympho..
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Awarded by Australian Academy of Science
Funding Acknowledgements
We thank all members of the Herold laboratory for their support and advice. G Siciliano, H Johnsons and their team for animal husbandry; S Monard and his team for help with flow cytometry; and D Tischner for help with RNA analysis. This work was supported by a Leukemia Foundation National Research Program PhD Scholarship (to RS), National Health and Medical Research Council, Australia (programme grant 1016701 and fellowship 1020363, to AS), project grant APP1049720 (to MJH). This work was made possible through Victorian State Government Operational Infrastructure Support and Australian Government National Health and Medical Research Council Independent Research Institutes Infrastructure Support Scheme. This work was supported by grants from the Austrian Science Fund (FWF), Grant I1298 (FOR-2036), the MCBO Doctoral College 'Molecular Cell Biology and Oncology' (W1101) and the 'Osterreichische Krebshilfe Tirol'. MDH and ST are supported by a DOC-fellowship from the Austrian Academy of Science (OAW).