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PMID: 14726496, 7867073, 7854420, 7939629
Consistent with the activation of nearly all RTKs, the ligands for the Tyro3 family of RTKs (Gas6 and protein S) and STK [macrophage-stimulating protein (MSP)] bind to the extracellular domain of their respective receptors, resulting in the up-regulation of kinase activity.</csml:comment>
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PMID: 14726496, 7867073, 7854420, 7939629
Consistent with the activation of nearly all RTKs, the ligands for the Tyro3 family of RTKs (Gas6 and protein S) and STK [macrophage-stimulating protein (MSP)] bind to the extracellular domain of their respective receptors, resulting in the up-regulation of kinase activity.</csml:comment>
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PMID: 14726496, 7867073, 7854420, 7939629
Consistent with the activation of nearly all RTKs, the ligands for the Tyro3 family of RTKs (Gas6 and protein S) and STK [macrophage-stimulating protein (MSP)] bind to the extracellular domain of their respective receptors, resulting in the up-regulation of kinase activity.</csml:comment>
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<csml:comments>
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</csml:comment>
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PMID: 14726496, 11081636
Listeria monocytogenes has been shown to gain entry into hepatocytes through the interaction of InlB with the Met receptor.</csml:comment>
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Indirect

</csml:comment>
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PMID: 14726496
signaling through the STK receptor regulates the activation of the alphaMbeta2 integrin, complement receptor 3 (CR3), which recognizes a variety of exogenous and endogenous ligands, including C3bi, intercellular adhesion molecule-1 (ICAM-1), LPS, and zymosan.</csml:comment>
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<csml:comment type="text">






PMID: 14726496
signaling through the STK receptor regulates the activation of the alphaMbeta2 integrin, complement receptor 3 (CR3), which recognizes a variety of exogenous and endogenous ligands, including C3bi, intercellular adhesion molecule-1 (ICAM-1), LPS, and zymosan.</csml:comment>
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PMID: 14726496
signaling through the STK receptor regulates the activation of the alphaMbeta2 integrin, complement receptor 3 (CR3), which recognizes a variety of exogenous and endogenous ligands, including C3bi, intercellular adhesion molecule-1 (ICAM-1), LPS, and zymosan.</csml:comment>
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PMID: 14726496
signaling through the STK receptor regulates the activation of the alphaMbeta2 integrin, complement receptor 3 (CR3), which recognizes a variety of exogenous and endogenous ligands, including C3bi, intercellular adhesion molecule-1 (ICAM-1), LPS, and zymosan.</csml:comment>
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PMID: 14726496
signaling through the STK receptor regulates the activation of the alphaMbeta2 integrin, complement receptor 3 (CR3), which recognizes a variety of exogenous and endogenous ligands, including C3bi, intercellular adhesion molecule-1 (ICAM-1), LPS, and zymosan.</csml:comment>
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Indirect
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PMID: 14726496, 11777982
MSP stimulation of primary peritoneal macrophages induces the expression of scavenger receptor A, which recognizes the exogenous ligands lipid A and lipoteichoic acid as well as oxidized low-density lipoprotein and apoptotic cells, resulting in enhanced uptake of acetylated LDL by these cells.</csml:comment>
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PMID: 14726496, 11777982
MSP stimulation of primary peritoneal macrophages induces the expression of scavenger receptor A, which recognizes the exogenous ligands lipid A and lipoteichoic acid as well as oxidized low-density lipoprotein and apoptotic cells, resulting in enhanced uptake of acetylated LDL by these cells.</csml:comment>
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PMID: 14726496, 11777982
MSP stimulation of primary peritoneal macrophages induces the expression of scavenger receptor A, which recognizes the exogenous ligands lipid A and lipoteichoic acid as well as oxidized low-density lipoprotein and apoptotic cells, resulting in enhanced uptake of acetylated LDL by these cells.</csml:comment>
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PMID: 14726496, 11777982
MSP stimulation of primary peritoneal macrophages induces the expression of scavenger receptor A, which recognizes the exogenous ligands lipid A and lipoteichoic acid as well as oxidized low-density lipoprotein and apoptotic cells, resulting in enhanced uptake of acetylated LDL by these cells.</csml:comment>
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PMID: 14726496
Although the Tyro3 family of receptors is reported to be widely expressed by monocytes and their derivatives, expression of the STK receptor by monocyte/macrophage populations is highly regulated.

PMID: 14726496, 10725742
LPS stimulation of macrophages in vitro or in vivo inhibits expression of STK.</csml:comment>
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Indirect

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PMID: 14726496, 11141491
STK may enhance clearance of Listeria through the activation of other PRRs, such as  R-A, which has been shown to be critical in the innate response to infection with Listeria.</csml:comment>
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<csml:comments>
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PMID: 14726496
MSP, the ligand for STK, was originally isolated from serum as a result of its ability to induce chemotaxis and complement-mediated phagocytosis by primary peritoneal macrophages.</csml:comment>
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PMID: 14726496, 7514598, 10586055, 12177064
MSP stimulation of primary peritoneal macrophages inhibits the production of nitric oxide (NO) and prostaglandin E2 in response to proinflammatory cytokines and LPS, as a result of an inhibition of the expression of inducible NO synthase (iNOS) and cyclooxygenase- 2, respectively.

PMID: 14726496, 10229863
Conversely, PI-3K has been shown to be a negative regulator of iNOS expression in macrophages through sustained activation of NF-kappaB.</csml:comment>
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<csml:comment type="text">



Indirect
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<csml:comment type="text">





PMID: 14726496, 7514598, 10586055, 12177064
MSP stimulation of primary peritoneal macrophages inhibits the production of nitric oxide (NO) and prostaglandin E2 in response to proinflammatory cytokines and LPS, as a result of an inhibition of the expression of inducible NO synthase (iNOS) and cyclooxygenase- 2, respectively.</csml:comment>
</csml:comments>
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<csml:comment type="text">



Indirect
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<csml:comment type="text">





PMID: 14726496, 7514598, 10586055, 12177064
MSP stimulation of primary peritoneal macrophages inhibits the production of nitric oxide (NO) and prostaglandin E2 in response to proinflammatory cytokines and LPS, as a result of an inhibition of the expression of inducible NO synthase (iNOS) and cyclooxygenase- 2, respectively.</csml:comment>
</csml:comments>
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</csml:comment>
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<csml:comment type="text">





PMID: 14726496, 7514598, 10586055, 12177064
MSP stimulation of primary peritoneal macrophages inhibits the production of nitric oxide (NO) and prostaglandin E2 in response to proinflammatory cytokines and LPS, as a result of an inhibition of the expression of inducible NO synthase (iNOS) and cyclooxygenase- 2, respectively.</csml:comment>
</csml:comments>
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PMID: 14726496, 10092806
A deletion in the tyrosine kinase domain of the closely related Mer RTK also results in enhanced sensitivity to endotoxic shock, and macrophages from these animals produce elevated levels of tumor necrosis factor alpha (TNF-alpha) and display increased activation of  NF-kappaB in response to stimulation with LPS.</csml:comment>
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PMID: 14726496, 10092806
A deletion in the tyrosine kinase domain of the closely related Mer RTK also results in enhanced sensitivity to endotoxic shock, and macrophages from these animals produce elevated levels of tumor necrosis factor alpha (TNF-alpha) and display increased activation of  NF-kappaB in response to stimulation with LPS.</csml:comment>
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PMID: 14726496, 10092806
A deletion in the tyrosine kinase domain of the closely related Mer RTK also results in enhanced sensitivity to endotoxic shock, and macrophages from these animals produce elevated levels of tumor necrosis factor alpha (TNF-alpha) and display increased activation of  NF-kappaB in response to stimulation with LPS.

PMID: 14726496, 10669740, 10485711
RTK signaling has been shown to activate NF-kappaB signaling in several cell types through the PI-3K- and Akt-dependent phosphorylation of IkappaB kinase.</csml:comment>
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PMID: 14726496, 11346799
In addition, Tyro3 receptors play a direct role in the recognition of apoptotic cells through the interaction of Gas6 with phosphatidyl serine on the surface of apoptotic cells, and macrophages from Mer knockout (KO) mice are defective in the clearance of apoptotic thymocytes.</csml:comment>
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PMID: 14726496
Although proinflammatory cytokines and LPS induce expression of iNOS, resulting in the metabolism of arginine to NO, T helper cell type 2 (Th2) cytokines induce expression of arginase, resulting in the production of ornithine.</csml:comment>
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PMID: 14726496
Although proinflammatory cytokines and LPS induce expression of iNOS, resulting in the metabolism of arginine to NO, T helper cell type 2 (Th2) cytokines induce expression of arginase, resulting in the production of ornithine.</csml:comment>
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PMID: 14726496
MSP stimulation of the STK receptor inhibits iNOS expression in response to interferon-gamma (IFN-gamma) and LPS and induces the expression of arginase, thus favoring the metabolism of arginine to ornithine.</csml:comment>
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PMID: 14726496
MSP stimulation of the STK receptor inhibits iNOS expression in response to interferon-gamma (IFN-gamma) and LPS and induces the expression of arginase, thus favoring the metabolism of arginine to ornithine.</csml:comment>
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PMID: 14726496, 11160269
IL-4, a potent inhibitor of NO production, accomplishes this task by up-regulating arginase expression through the activation of signal transducer and activator of transcription (Stat)6 and limiting the amount of L-arginine available to iNOS.

PMID: 14726496
The ability of STK and PI-3K to induce arginase I expression in resident macrophages suggests a potential dual role for RTK signaling in limiting tissue-destructive inflammation and pro-moting the wound-healing process by tipping the balance of arginine metabolism in macrophages.</csml:comment>
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PMID: 14726496, 11160269
IL-4, a potent inhibitor of NO production, accomplishes this task by up-regulating arginase expression through the activation of signal transducer and activator of transcription (Stat)6 and limiting the amount of L-arginine available to iNOS.

PMID: 14726496, 1777982
We have shown that MSP induces expression of arginase I in primary peritoneal macrophages and cooperates with IL-4 to enhance arginase activity in a Stat6-dependent manner.</csml:comment>
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PMID: 14726496
pretreatment of primary peritoneal macrophages with MSP for 2&#8211;4 h results in the complete inhibition of IL-12 production in response to IFN-gamma and LPS as a result of the inhibition of IL-12 p40 expression.

PMID: 14726496, 12154357
recent studies have demonstrated that PI-3K negatively regulates the production of IL-12 by dendritic cells and Th1 responses in vivo.</csml:comment>
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Indirect</csml:comment>
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PMID: 14726496
pretreatment of primary peritoneal macrophages with MSP for 2&#8211;4 h results in the complete inhibition of IL-12 production in response to IFN-gamma and LPS as a result of the inhibition of IL-12 p40 expression.

PMID: 14726496
This inhibition appears to result from a block in Stat1 tyrosine phosphorylation and IFN consensus sequence-binding protein up-regulation induced by IFN-gamma.

PMID: 14726496, 12154357
recent studies have demonstrated that PI-3K negatively regulates the production of IL-12 by dendritic cells and Th1 responses in vivo.</csml:comment>
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PMID: 14726496
Pretreatment of macrophages with MSP also results in the inhibition of major histcompatibility complex (MHC) class II expression in response to IFN-gamma and IL-4 and reduced Th1/Th2 differentiation under polarizing conditions in vitro.</csml:comment>
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Indirect</csml:comment>
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PMID: 14726496
Pretreatment of macrophages with MSP also results in the inhibition of major histcompatibility complex (MHC) class II expression in response to IFN-gamma and IL-4 and reduced Th1/Th2 differentiation under polarizing conditions in vitro.</csml:comment>
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PMID: 14726496
This inhibition appears to result from a block in Stat1 tyrosine phosphorylation and IFN consensus sequence-binding protein up-regulation induced by IFN-gamma.

PMID: 14726496
RTK signaling could ultimately inhibit LPS-induced NF-kappaB activation and IFN-gamma-induced Stat1 tyrosine phosphorylation through the induction of classical negative-feedback pathways.</csml:comment>
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Indirect</csml:comment>
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PMID: 14726496, 11452127
macrophages and dendritic cells from triple mutant mice for the RTKs Tyro3, Axl, and Mer express elevated levels of MHC class II and the costimulatory molecule B7-2 in response to LPS and produce increased levels of IL-12.</csml:comment>
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Indirect</csml:comment>
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<csml:comment type="text">



PMID: 14726496
IL-10, a potent inhibitor of classical activation, induces Stat3 phosphorylation.</csml:comment>
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Indirect</csml:comment>
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PMID: 14726496, 12538698, 10029571
IL-10 induces the expression of SOCS1 and SOCS3 in a Stat3-dependent manner.</csml:comment>
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Indirect</csml:comment>
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PMID: 14726496, 12538698, 10029571
IL-10 induces the expression of SOCS1 and SOCS3 in a Stat3-dependent manner.</csml:comment>
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Indirect</csml:comment>
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<csml:comment type="text">



PMID: 14726496
the induction of IL-10 in response to LPS may provide an important negative-feedback mechanism for limiting the extent and/or duration of this response.</csml:comment>
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Indirect
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<csml:comment type="text">



PMID: 14726496
Several RTKs have also been shown to induce the expression of SOCS proteins, suggesting the possibility that RTK signaling could regulate macrophage activation through the induction of SOCS1 and SOCS3.</csml:comment>
</csml:comments>
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</csml:comment>
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Indirect</csml:comment>
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</csml:comment>
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<csml:comment type="text">


PMID: 14726496, 10669740, 10485711
RTK signaling has been shown to activate NF-kappaB signaling in several cell types through the PI-3K- and Akt-dependent phosphorylation of IkappaB kinase.</csml:comment>
</csml:comments>
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PMID: 14726496, 10669740, 10485711
RTK signaling has been shown to activate NF-kappaB signaling in several cell types through the PI-3K- and Akt-dependent phosphorylation of IkappaB kinase.</csml:comment>
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Indirect</csml:comment>
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PMID: 14726496
Twist 1 and twist 2 are basichelix-loop-helix transcription factors that are up-regulated in response to NF-kappaB.

PMID: 14726496
Negative-feedback inhibition of the NF-kappaB signaling pathway has also been demonstrated through the up-regulation of IkappaB and more recently, the p65-dependent xpression of twist proteins.</csml:comment>
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Indirect</csml:comment>
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PMID: 14726496
Twist 1 and twist 2 are basichelix-loop-helix transcription factors that are up-regulated in response to NF-kappaB.

PMID: 14726496
Negative-feedback inhibition of the NF-kappaB signaling pathway has also been demonstrated through the up-regulation of IkappaB and more recently, the p65-dependent xpression of twist proteins.</csml:comment>
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<csml:comment type="text">



PMID: 14726496
Negative-feedback inhibition of the NF-kappaB signaling pathway has also been demonstrated through the up-regulation of IkappaB and more recently, the p65-dependent xpression of twist proteins.</csml:comment>
</csml:comments>
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PMID: 14726496, 10825239, 11169739
It is interesting that the Met RTK has been shown to induce muscle differentiation through the upregulation of twist 1 expression, and fibroblast growth factor 2 induces expression of twist 1 in osteoblasts.</csml:comment>
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Indirect</csml:comment>
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PMID: 14726496, 10825239, 11169739
It is interesting that the Met RTK has been shown to induce muscle differentiation through the upregulation of twist 1 expression, and fibroblast growth factor 2 induces expression of twist 1 in osteoblasts.PMID: 14726496, 10825239, 11169739
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Indirect</csml:comment>
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PMID: 14726496
IL-12 has been shown to play an important role in sustaining autoimmunity in several mouse models through its ability to mediate the production of IFN-gamma and favor a Th1 response.</csml:comment>
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PMID: 14726496
IL-12 has been shown to play an important role in sustaining autoimmunity in several mouse models through its ability to mediate the production of IFN-gamma and favor a Th1 response.</csml:comment>
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PMID: 14726496
Pretreatment of macrophages with MSP also results in the inhibition of major histcompatibility complex (MHC) class II expression in response to IFN-gamma and IL-4 and reduced Th1/Th2 differentiation under polarizing conditions in vitro.</csml:comment>
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<csml:comment type="text">


PMID: 14726496, 11160269
IL-4, a potent inhibitor of NO production, accomplishes this task by up-regulating arginase expression through the activation of signal transducer and activator of transcription (Stat)6 and limiting the amount of L-arginine available to iNOS.</csml:comment>
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PMID: 14726496, 10825239, 11169739
It is interesting that the Met RTK has been shown to induce muscle differentiation through the upregulation of twist 1 expression, and fibroblast growth factor 2 induces expression of twist 1 in osteoblasts.PMID: 14726496, 10825239, 11169739</csml:comment>
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PMID: 14726496
Several RTKs have also been shown to induce the expression of SOCS proteins, suggesting the possibility that RTK signaling could regulate macrophage activation through the induction of SOCS1 and SOCS3.</csml:comment>
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PMID: 14726496
pretreatment of primary peritoneal macrophages with MSP for 2&#8211;4 h results in the complete inhibition of IL-12 production in response to IFN-gamma and LPS as a result of the inhibition of IL-12 p40 expression.

PMID: 14726496
This inhibition appears to result from a block in Stat1 tyrosine phosphorylation and IFN consensus sequence-binding protein up-regulation induced by IFN-gamma.

PMID: 14726496, 12154357
recent studies have demonstrated that PI-3K negatively regulates the production of IL-12 by dendritic cells and Th1 responses in vivo.</csml:comment>
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PMID: 14726496
Although proinflammatory cytokines and LPS induce expression of iNOS, resulting in the metabolism of arginine to NO, T helper cell type 2 (Th2) cytokines induce expression of arginase, resulting in the production of ornithine.</csml:comment>
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