Involvement of nuclear factor of activated T cells in granulocyte-macrophage colony-stimulating factor production in canine keratinocytes stimulated with a cysteine protease

2013 ◽  
Vol 24 (3) ◽  
pp. 310-e69 ◽  
Author(s):  
Tsuyoshi Kimura ◽  
Machiko Sekido ◽  
Aki Iio ◽  
Naoki Chimura ◽  
Sanae Shibata ◽  
...  
Keyword(s):  
T Cells ◽  
Cysteine Protease ◽  
Nuclear Factor ◽  
Colony Stimulating Factor ◽  
Activated T Cells ◽  
Factor Production ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

scholarly journals Hematopoiesis in mice lacking the entire granulocyte-macrophage colony- stimulating factor/interleukin-3/interleukin-5 functions

Blood ◽  
1996 ◽  
Vol 88 (7) ◽  
pp. 2458-2464 ◽  
Author(s):  
R Nishinakamura ◽  
A Miyajima ◽  
PJ Mee ◽  
VL Tybulewicz ◽  
R Murray
Keyword(s):  
T Cells ◽  
Double Mutant ◽  
Mutant Mice ◽  
Colony Stimulating Factor ◽  
Activated T Cells ◽  
Interleukin 3 ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-5 are major hematopoietic cytokines produced by activated T cells and exhibit similar biologic activities by signaling through a common receptor subunit (beta c). Mice lacking beta c show a pulmonary alveolar proteinosis-like disease and reduced numbers of peripheral eosinophils, which are explained by the lack of GM-CSF and IL-5 function, respectively. However, beta c-deficient hematopoietic cells do respond to IL-3 normally, probably through an additional beta subunit of the IL-3 receptor (beta IL3) that is present in the mouse. Thus, almost normal hematopoiesis in beta c-deficient mice may be caused by functional redundancy between IL-3 and GM-CSF. To clarify the role of the entire IL-3/GM-CSF/IL-5 system in hematopoiesis in vivo, we crossed the beta c mutant mice with mice deficient for IL-3 ligand to generate mice lacking the entire IL-3/GM-CSF/IL-5 functions. The double-mutant mice were apparently normal and fertile. The severity of the lung pathology in the beta c/IL-3 double-mutant mice showed normal hemodynamic parameters except for reduced numbers of eosinophils and the lack of eosinophilic response to parasites, which were also found in beta c mutant mice. The immune response of the beta c/IL-3 double-mutant mice to Listeria mono-cytogenes was normal, as was hematopoietic recovery after administration of the cytotoxic drug, 5-fluorouracil. Although it has been believed that IL-3/GM-CSF/IL-5 produced by activated T cells play a major role in expansion of hematopoietic cells in emergency, our results indicate that the entire function of IL-3/GM- CSF/IL-5 is dispensable for hematopoiesis in emergency as well as in the steady state. Thus, there must be an alternative mechanism to produce blood cells in both situations.

scholarly journals Macrophage colony-stimulating factor (CSF-1) gene expression in human T- lymphocyte clones

Blood ◽  
1991 ◽  
Vol 77 (4) ◽  
pp. 780-786 ◽  
Author(s):  
MM Hallet ◽  
V Praloran ◽  
H Vie ◽  
MA Peyrat ◽  
G Wong ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Phenotypic Diversity ◽  
Calcium Ionophore ◽  
Colony Stimulating Factor ◽  
T Cell Clones ◽  
Cell Clones ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract Macrophage colony stimulating factor (CSF-1) is one of several cytokines that control the differentiation, survival, and proliferation of monocytes and macrophages. A set of 11 human T-cell clones, chosen for their phenotypic diversity, were tested for their ability to express CSF-1 mRNA. After 5 hours of stimulation with phorbol myristate acetate (PMA) + calcium ionophore (Cal), all T-cell clones expressed a major 4-kb transcript, a less abundant 2-kb transcript, and several other minor species. This pattern of expression is typical for CSF-1 mRNAs. Furthermore, of the two alloreactive T-cell clones analyzed, only one showed a definitive message for CSF-1 on specific antigenic stimulation, but with delayed kinetics and less efficiency. Both conditions of stimulation induced the release of CSF-1 protein by T cells in the culture medium. Together, these findings demonstrate for the first time that normal T cells are able to produce CSF-1, previous reports being limited to two cases of tumoral cells of the T-cell lineage.

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