CSF-Deficient Mice — What Have They Taught Us?

  1. Gregory R. Bock Organizer and
  2. Jamie A. Goode
  1. Graham J. Lieschke

Published Online: 28 SEP 2007

DOI: 10.1002/9780470515280.ch5

Ciba Foundation Symposium 204 - The Molecular Basis of Cellular Defence Mechanisms

Ciba Foundation Symposium 204 - The Molecular Basis of Cellular Defence Mechanisms

How to Cite

Lieschke, G. J. (2007) CSF-Deficient Mice — What Have They Taught Us?, in Ciba Foundation Symposium 204 - The Molecular Basis of Cellular Defence Mechanisms (eds G. R. Bock and J. A. Goode), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470515280.ch5

Author Information

  1. Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142–1479, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471965671

Online ISBN: 9780470515280

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Keywords:

  • CSF-deficient mice;
  • haemopoiesis;
  • gene targeting;
  • redundancy;
  • haemopoietic cell populations

Summary

Haemopoietic growth factor-deficient mice have been particularly instructive for defining the usual physiological role of these factors. Mice now exist lacking the granulopoietic factors G-CSF, GM-CSF, M-CSF (CSF-1), SCF, several other factors influencing haemopoiesis (including erythropoietin, interleukins 5 and 6), combinations of these factors (GM- & M-CSF; G- & GM-CSF; G- & GM- & M-CSF) and several CSF receptor components. Most of these mice were generated by targeted gene disruption, others are spontaneously arising mutants. The phenotypes of these mice indicate that the granulopoietic factors have both unique and redundant roles in vivo. Some factors are uniquely important in baseline myelopoiesis. Experimental infection of CSF-deficient mice indicates unique roles for some factors in emergency ‘overdrive’ haemopoiesis. Recovery from myeloablation evaluates the role of CSFs in emergency ‘restoring normality’ haemopoiesis. Redundancy also exists in the capacity of CSFs to support complete granulocyte development in vivo. Some factors are not involved in all the in vivo roles suggested by the range of their actions demonstrable in vitro. Some CSFs have indispensable roles in non-haemopoietic tissues. Some factors have in vivo roles not anticipated from previous studies. Mice deficient in several factors have identified compensating roles for factors by revealing exacerbated and additional phenotypic features, and may unmask additional in vivo roles.