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Interleukin‐10 and interferon‐γ modulate surface expression of fractalkine‐receptor (CX 3 CR1) via PI3K in monocytes
Author(s) -
Ramos María V.,
Fernández Gabriela C.,
Brando Romina J. Fernández,
Panek Cecilia A.,
Bentancor Leticia V.,
Landoni Verónica I.,
Isturiz Martín A.,
Palermo Marina S.
Publication year - 2010
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2009.03181.x
Subject(s) - chemotaxis , monocyte , chemokine , microbiology and biotechnology , receptor , biology , cell surface receptor , inflammation , chemistry , immunology , biochemistry
Summary The membrane‐anchored form of the chemokine fractalkine (CX 3 CL1) has been identified as a novel adhesion molecule that interacts with its specific receptor (CX 3 CR1) expressed in monocytes, T cells and natural killer cells to induce adhesion. In addition, CX 3 CL1 can be cleaved from the cell membrane to induce chemotaxis of CX 3 CR1‐expressing leucocytes. Recently, marked variations in CX 3 CR1 monocyte expression have been observed during several pathological conditions. Regulation of CX 3 CR1 in monocytes during basal or inflammatory/anti‐inflammatory conditions is poorly understood. The aim of this study was therefore to examine CX 3 CR1 expression during monocyte maturation and the effect of soluble mediators on this process. We found that basal expression of CX 3 CR1 in fresh monocytes was reduced during culture, and that lipopolysacchairde accelerated this effect. In contrast, interleukin‐10 and interferon‐γ treatment abrogated CX 3 CR1 down‐modulation, through a phosphatidylinositol 3 kinase‐dependent pathway. Most importantly, CX 3 CR1 membrane expression correlated with monocyte CX 3 CL1‐dependent function. Taken together, our data demonstrate that CX 3 CR1 expression in monocytes can be modulated, and suggest that alterations in their environment are able to influence CX 3 CL1‐dependent functions, such as chemotaxis and adhesion, leading to changes in the kinetics, composition and/or functional status of the leucocyte infiltrate.