m-csf and gm-csf regulation of stat5 activation and dna binding in myeloid cell differentiation is disrupted in nonobese diabetic mice

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ID: 182206
2008
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Abstract
Defects in macrophage colony-stimulating factor (M-CSF) signaling disrupt myeloid cell differentiation in nonobese diabetic (NOD) mice, blocking myeloid maturation into tolerogenic antigen-presenting cells (APCs). In the absence of M-CSF signaling, NOD myeloid cells have abnormally high granulocyte macrophage colony-stimulating factor (GM-CSF) expression, and as a result, persistent activation of signal transducer/activator of transcription 5 (STAT5). Persistent STAT5 phosphorylation found in NOD macrophages is not affected by inhibiting GM-CSF. However, STAT5 phosphorylation in NOD bone marrow cells is diminished if GM-CSF signaling is blocked. Moreover, if M-CSF signaling is inhibited, GM-CSF stimulation in vitro can promote STAT5 phosphorylation in nonautoimmune C57BL/6 mouse bone marrow cultures to levels seen in the NOD. These findings suggest that excessive GM-CSF production in the NOD bone marrow may interfere with the temporal sequence of GM-CSF and M-CSF signaling needed to mediate normal STAT5 function in myeloid cell differentiation gene regulation.
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rumore-maton2008clinicalm-csf Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;B. Rumore-Maton;J. Elf;N. Belkin;B. Stutevoss;F. Seydel;E. Garrigan;S. A. Litherland
Journal Applied Surface Science
Year 2008
DOI
10.1155/2008/769795
URL
http://dx.doi.org/10.1155/2008/769795
Keywords
immunologic diseases allergy

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