T cell survival and function requires the c-Abl tyrosine kinase

Isabelle Silberman, Ronit Vogt Sionov, Valentina Zuckerman, Sue Haupt, Zehavit Goldberg, Andreas Strasser, Zami S. Ben-Sasson, Michal Baniyash, Anthony J. Koleske, Ygal Haupt*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


C-Abl (Abl) regulates multiple cellular processes, including proliferation, survival, shape determination and motility, and participates in cellular responses to genotoxic and oxidative stress stimuli. Mice lacking Abl exhibit retarded growth, osteoporosis and defects in the immune system resulting in lymphopoenia and susceptibility to infections, leading to early death. To define the role of Abl in the regulation of adult T cells we ablated Abl exclusively in T cells by generating mice with floxed abl alleles and expressing an Lck-Cre transgene (Abl-T-/-). These mice exhibited thymic atrophy and abnormally reduced T cell numbers in the periphery. The thymic atrophy was caused by increased susceptibility of thymocytes to cell death. Importantly, Abl deficient T cells displayed abnormally reduced response to mitogenic stimulation in vitro. Consequently, Abl-T-/- mice exhibited impaired ability to reject syngeneic tumor, to induce T-mediated tumor cell killing, and to generate anti-tumor antibodies. These results demonstrate a cell-autonomous role for Abl in T cell function and survival.

Original languageAmerican English
Pages (from-to)3847-3857
Number of pages11
JournalCell Cycle
Issue number24
StatePublished - 15 Dec 2008

Bibliographical note

Funding Information:
We thank E. Galun and E. Zeira for their assistant with the bioluminescence analysis, E. Pikarsky for histological examinations, O. Alsheich-Bartok for assistance with microscopy, M. Ratner for technical assistance, E. Yefenof, A. Kruisbeek and A. Honigman for expression plasmids and cells, D. Wallach and T-B. Kang for FasL and E. Pikarsky and E. Zeira for comments on the manuscript. This work was supported by grants from the Association for International Cancer Research, the German-Israeli Foundation for Scientific Research and Development, the Israel Cancer Association, the Israel Science Foundation (grant No. 1341/05), and by EC FP6 funding of the European Commission (contract 503576). This publication reflects only the author’s views. The European Commission is not liable for any use that may be made of the information herein.


  • Apoptosis
  • Mitogenic activation
  • T cell
  • Tumor rejection
  • c-Abl


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