Overexpression of Batf induces an apoptotic defect and an associated lymphoproliferative disorder in mice

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Abstract

Activator protein-1 (AP-1) is a dimeric transcription factor composed of the Jun, Fos and Atf families of proteins. Batf is expressed in the immune system and participates in AP-1 dimers that modulate gene expression in response to a variety of stimuli. Transgenic (Tg) mice overexpressing human BATF in T cells were generated using the human CD2 promoter (CD2-HA (hemagglutinin antigen)-BATF). By 1 year of age, over 90% of the mice developed a lymphoproliferative disorder (LPD). The enlarged lymph nodes characteristic of this LPD contain a polyclonal accumulation of T cells with a CD4+ bias, yet efforts to propagate these tumor cells in vitro demonstrate that they do not proliferate as well as wild-type CD4+ T cells. Instead, the accumulation of these cells is likely due to an apoptotic defect as CD2-HA-BATF Tg T cells challenged by trophic factor withdrawal in vitro resist apoptosis and display a pro-survival pattern of Bcl-2 family protein expression. As elevated levels of Batf expression are a feature of lymphoid tumors in both humans and mice, these observations support the use of CD2-HA-BATF mice as a model for investigating the molecular details of apoptotic dysregulation in LPD. © 2012 Macmillan Publishers Limited All rights reserved.

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Logan, M. R., Jordan-Williams, K. L., Poston, S., Liao, J., & Taparowsky, E. J. (2012). Overexpression of Batf induces an apoptotic defect and an associated lymphoproliferative disorder in mice. Cell Death and Disease, 3(5). https://doi.org/10.1038/cddis.2012.49

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