Induction of macrophage-derived chemokine/CCL22 expression in experimental autoimmune encephalomyelitis and cultured microglia: implications for disease regulation

Macrophage-derived chemokine (MDC/CCL22) and its receptor CCR4 have been implicated in chronic inflammatory processes and in the homing of monocytes, Th2 cells and regulatory T-cell subsets. Here, we demonstrate that MDC and CCR4 mRNAs are expressed in the central nervous system (CNS) of mice develo...

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Bibliographic Details
Published in:Journal of neuroimmunology 2002-09, Vol.130 (1), p.10-21
Main Authors: Columba-Cabezas, Sandra, Serafini, Barbara, Ambrosini, Elena, Sanchez, Massimo, Penna, Giuseppe, Adorini, Luciano, Aloisi, Francesca
Format: Article
Language:English
Subjects:
Animals
Astrocytes - drug effects
Astrocytes - immunology
Astrocytes - metabolism
Brain
Cells, Cultured
Central Nervous System - immunology
Central Nervous System - metabolism
Central Nervous System - physiopathology
Chemokine CCL22
Chemokines
Chemokines, CC - genetics
Chemokines, CC - immunology
Chemokines, CC - metabolism
EAE
Encephalomyelitis, Autoimmune, Experimental - immunology
Encephalomyelitis, Autoimmune, Experimental - physiopathology
Female
Gene Expression Regulation - immunology
Glia
Immunohistochemistry
Macrophages - cytology
Macrophages - immunology
Macrophages - metabolism
Mice
Mice, Inbred Strains
Microglia - drug effects
Microglia - immunology
Microglia - metabolism
Multiple Sclerosis - immunology
Multiple Sclerosis - physiopathology
Receptors, CCR4
Receptors, Chemokine - genetics
Receptors, Chemokine - immunology
Receptors, Chemokine - metabolism
RNA, Messenger - metabolism
Th1/Th2
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Summary:Macrophage-derived chemokine (MDC/CCL22) and its receptor CCR4 have been implicated in chronic inflammatory processes and in the homing of monocytes, Th2 cells and regulatory T-cell subsets. Here, we demonstrate that MDC and CCR4 mRNAs are expressed in the central nervous system (CNS) of mice developing relapsing–remitting and chronic–relapsing forms of experimental autoimmune encephalomyelitis (EAE). By immunohistochemistry, we show that MDC is produced by CNS-infiltrating leukocytes and intraparenchymal microglia, whereas CCR4 is expressed on some invading leukocytes. Upon in vitro activation, mouse microglia express MDC transcripts and secrete bioactive MDC that induces chemotaxis of Th2, but not Th1 cells. We suggest that MDC produced by microglia could regulate Th1-mediated CNS inflammation by facilitating the homing of Th2 and, possibly, regulatory T cells into the lesion site.
ISSN:0165-5728
1872-8421
DOI:10.1016/S0165-5728(02)00170-4