Type II-activated macrophages suppress the development of experimental autoimmune encephalomyelitis

Treatment with immune complexes, which ligate Fcγ receptors (FcγRs), suppresses the development of experimental autoimmune encephalomyelitis (EAE). To determine the mechanism of action, we investigated how these immune complexes affected type II activation of macrophages (that is, exposure to immune...

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Bibliographic Details
Published in:Immunology and cell biology 2009-03, Vol.87 (3), p.235-240
Main Authors: Tierney, Joanna B, Kharkrang, Marie, La Flamme, Anne Camille
Format: Article
Language:English
Subjects:
Animals
Antigen-Antibody Complex - administration & dosage
autoimmunity
B7-1 Antigen - drug effects
B7-1 Antigen - immunology
B7-1 Antigen - metabolism
B7-H1 Antigen
CD40 Antigens - antagonists & inhibitors
CD40 Antigens - immunology
CD40 Antigens - metabolism
Down-Regulation - drug effects
Down-Regulation - immunology
EAE
Encephalomyelitis, Autoimmune, Experimental - immunology
Encephalomyelitis, Autoimmune, Experimental - prevention & control
Fc receptors
Glycoproteins - pharmacology
immune complexes
Immunologic Factors - administration & dosage
Interferon-gamma - pharmacology
Interleukin-10 - biosynthesis
Interleukin-10 - immunology
Interleukin-12 Subunit p40 - biosynthesis
Interleukin-12 Subunit p40 - immunology
Lipopolysaccharides - immunology
macrophage
Macrophage Activation
Macrophages - drug effects
Macrophages - immunology
Membrane Glycoproteins - antagonists & inhibitors
Membrane Glycoproteins - immunology
Membrane Glycoproteins - metabolism
Mice
Mice, Inbred C57BL
Myelin-Oligodendrocyte Glycoprotein
Peptide Fragments - pharmacology
Peptides - antagonists & inhibitors
Peptides - immunology
Peptides - metabolism
Receptors, IgG - immunology
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Summary:Treatment with immune complexes, which ligate Fcγ receptors (FcγRs), suppresses the development of experimental autoimmune encephalomyelitis (EAE). To determine the mechanism of action, we investigated how these immune complexes affected type II activation of macrophages (that is, exposure to immune complexes in a proinflammatory environment). Our results show that lower doses of interferon‐γ (IFN‐γ) were more effective at priming bone marrow‐derived macrophages (BMMφ) to produce more interleukin 10 (IL‐10) and less IL‐12p40 in response to lipopolysaccharide (LPS) and immune complexes compared with LPS alone. Moreover, at the lowest level of IFN‐γ (20 U ml−1), a significant downregulation in the surface expression of CD40, CD80 and PD‐L1 was observed in LPS and immune complex‐stimulated macrophages (that is, type II activated) than macrophages stimulated with LPS alone (that is, classically activated). Finally, treatment of mice with type II‐activated macrophages protected them from developing EAE, suggesting that administration of immune complexes is protective against EAE by inducing type II‐activated macrophages.
ISSN:0818-9641
1440-1711
DOI:10.1038/icb.2008.99