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.