Abnormal Stat Activation, Hematopoietic Homeostasis, and Innate Immunity in c-fes−/− Mice
2000; Cell Press; Volume: 13; Issue: 3 Linguagem: Inglês
10.1016/s1074-7613(00)00039-x
ISSN1097-4180
AutoresRenée Hackenmiller, Juyong Brian Kim, Ricardo A. Feldman, M. Celeste Simon,
Tópico(s)T-cell and B-cell Immunology
ResumoThe c-fes protooncogene encodes a nonreceptor tyrosine kinase (Fes) implicated in cytokine receptor signal transduction, neutrophil survival, and myeloid differentiation. To determine the role of Fes in embryonic development and hematopoiesis, we engineered a null mutation of the murine c-fes locus. c-fes-/- mice are viable but not born in the expected Mendelian ratios. Live born c-fes-/- mice exhibit lymphoid/myeloid homeostasis defects, compromised innate immunity, and increased Stat activation in response to GM-CSF and IL-6 signaling. Therefore, increased cytokine responsiveness in the absence of Fes leads to abnormal myeloid proliferation and functional defects in the macrophage lineage.
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