IMEX   05356
INSTITUTO DE MEDICINA EXPERIMENTAL
Unidad Ejecutora - UE
artículos
Título:
Il-10 And INF-ã Modulate Surface Expression Of Fractalkine-Receptor (Cx3cr1) In Monocytes Via Pi3k
Autor/es:
RAMOS M.V; FERNANDEZ G.C; FERNANDEZ-BRANDO R.J; PANEK CA; BENTANCOR LV; LANDONI V.I; ISTURIZ M.A; PALERMO M.S
Revista:
IMMUNOLOGY
Referencias:
Año: 2009
ISSN:
0019-2805
Resumen:
SUMMARY The membrane anchored-form of the chemokine fractalkine (CX3CL1) has been identified as a novel adhesion molecule that interacts with its specific receptor (CX3CR1) expressed on monocytes, T and natural killer cells to induce adhesion. In addition, CX3CL1 can be cleaved from the cell membrane to induce chemotaxis of CX3CR1-expressing leukocytes. Recently, it has been reported marked variations in CX3CR1-monocyte expression during several pathologic conditions. Thus far, it is poorly understood how the CX3CR1 is regulated in monocytes during basal or inflammatory/anti-inflammatory conditions. The aim of this study was to examine the CX3CR1-expression during monocyte maturation and the effect of soluble mediators on this process. Our data indicate that basal expression of CX3CR1 on fresh monocytes is reduced during culture, and LPS or TNF-á accelerated this effect. On the contrary, IL-10 and IFN-ã treatment abrogated CX3CR1 down-modulation, through a PI3K-dependent pathway. Most important, CX3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CL1) has been identified as a novel adhesion molecule that interacts with its specific receptor (CX3CR1) expressed on monocytes, T and natural killer cells to induce adhesion. In addition, CX3CL1 can be cleaved from the cell membrane to induce chemotaxis of CX3CR1-expressing leukocytes. Recently, it has been reported marked variations in CX3CR1-monocyte expression during several pathologic conditions. Thus far, it is poorly understood how the CX3CR1 is regulated in monocytes during basal or inflammatory/anti-inflammatory conditions. The aim of this study was to examine the CX3CR1-expression during monocyte maturation and the effect of soluble mediators on this process. Our data indicate that basal expression of CX3CR1 on fresh monocytes is reduced during culture, and LPS or TNF-á accelerated this effect. On the contrary, IL-10 and IFN-ã treatment abrogated CX3CR1 down-modulation, through a PI3K-dependent pathway. Most important, CX3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CR1) expressed on monocytes, T and natural killer cells to induce adhesion. In addition, CX3CL1 can be cleaved from the cell membrane to induce chemotaxis of CX3CR1-expressing leukocytes. Recently, it has been reported marked variations in CX3CR1-monocyte expression during several pathologic conditions. Thus far, it is poorly understood how the CX3CR1 is regulated in monocytes during basal or inflammatory/anti-inflammatory conditions. The aim of this study was to examine the CX3CR1-expression during monocyte maturation and the effect of soluble mediators on this process. Our data indicate that basal expression of CX3CR1 on fresh monocytes is reduced during culture, and LPS or TNF-á accelerated this effect. On the contrary, IL-10 and IFN-ã treatment abrogated CX3CR1 down-modulation, through a PI3K-dependent pathway. Most important, CX3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CL1 can be cleaved from the cell membrane to induce chemotaxis of CX3CR1-expressing leukocytes. Recently, it has been reported marked variations in CX3CR1-monocyte expression during several pathologic conditions. Thus far, it is poorly understood how the CX3CR1 is regulated in monocytes during basal or inflammatory/anti-inflammatory conditions. The aim of this study was to examine the CX3CR1-expression during monocyte maturation and the effect of soluble mediators on this process. Our data indicate that basal expression of CX3CR1 on fresh monocytes is reduced during culture, and LPS or TNF-á accelerated this effect. On the contrary, IL-10 and IFN-ã treatment abrogated CX3CR1 down-modulation, through a PI3K-dependent pathway. Most important, CX3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CR1-expressing leukocytes. Recently, it has been reported marked variations in CX3CR1-monocyte expression during several pathologic conditions. Thus far, it is poorly understood how the CX3CR1 is regulated in monocytes during basal or inflammatory/anti-inflammatory conditions. The aim of this study was to examine the CX3CR1-expression during monocyte maturation and the effect of soluble mediators on this process. Our data indicate that basal expression of CX3CR1 on fresh monocytes is reduced during culture, and LPS or TNF-á accelerated this effect. On the contrary, IL-10 and IFN-ã treatment abrogated CX3CR1 down-modulation, through a PI3K-dependent pathway. Most important, CX3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CR1-monocyte expression during several pathologic conditions. Thus far, it is poorly understood how the CX3CR1 is regulated in monocytes during basal or inflammatory/anti-inflammatory conditions. The aim of this study was to examine the CX3CR1-expression during monocyte maturation and the effect of soluble mediators on this process. Our data indicate that basal expression of CX3CR1 on fresh monocytes is reduced during culture, and LPS or TNF-á accelerated this effect. On the contrary, IL-10 and IFN-ã treatment abrogated CX3CR1 down-modulation, through a PI3K-dependent pathway. Most important, CX3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CR1 is regulated in monocytes during basal or inflammatory/anti-inflammatory conditions. The aim of this study was to examine the CX3CR1-expression during monocyte maturation and the effect of soluble mediators on this process. Our data indicate that basal expression of CX3CR1 on fresh monocytes is reduced during culture, and LPS or TNF-á accelerated this effect. On the contrary, IL-10 and IFN-ã treatment abrogated CX3CR1 down-modulation, through a PI3K-dependent pathway. Most important, CX3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CR1-expression during monocyte maturation and the effect of soluble mediators on this process. Our data indicate that basal expression of CX3CR1 on fresh monocytes is reduced during culture, and LPS or TNF-á accelerated this effect. On the contrary, IL-10 and IFN-ã treatment abrogated CX3CR1 down-modulation, through a PI3K-dependent pathway. Most important, CX3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CR1 on fresh monocytes is reduced during culture, and LPS or TNF-á accelerated this effect. On the contrary, IL-10 and IFN-ã treatment abrogated CX3CR1 down-modulation, through a PI3K-dependent pathway. Most important, CX3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.ã treatment abrogated CX3CR1 down-modulation, through a PI3K-dependent pathway. Most important, CX3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CR1-membrane expression correlated with monocyte CX3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CL1-dependent function. Together, our data demonstrate that CX3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.3CL1-dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetic, composition and/or functional status of the leukocyte infiltrate.