Interferon-gamma produced by encephalitogenic cells induces suppressors of cytokine signaling in primary murine astrocytes

Suppressors of cytokine signaling (SOCS) are proteins that modulate cytokine responses in lymphoid cells. In these studies, cultured primary mouse astrocytes expressed SOCS-3 mRNA constitutively. Treatment with interferon-gamma (IFN-g) induced SOCS-1 and enhanced SOCS-3 expression, and was associate...

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Published inJournal of neuroimmunology Vol. 151; no. 1; pp. 195 - 200
Main Authors Stark, Jennifer L, Lyons, Jeri-Anne, Cross, Anne H
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.06.2004
Subjects
Animals
Astrocytes
Astrocytes - immunology
Astrocytes - metabolism
Carrier Proteins - biosynthesis
Cells, Cultured
Encephalomyelitis, Autoimmune, Experimental - immunology
Experimental autoimmune encephalomyelitis
Gene Expression - immunology
Immune regulation
Interferon gamma
Interferon-gamma - immunology
Interleukin-6 - biosynthesis
Leukemia Inhibitory Factor
Mice
Myelin Basic Protein - immunology
Repressor Proteins - biosynthesis
RNA, Messenger - analysis
Suppressor of Cytokine Signaling 1 Protein
Suppressor of Cytokine Signaling 3 Protein
Suppressor of Cytokine Signaling Proteins
Suppressors of cytokine signaling
Transcription Factors - biosynthesis
Tumor Necrosis Factor-alpha - biosynthesis
Experimental autoimmune encephalomyelitis
Suppressors of cytokine signaling
Immune regulation
Astrocytes
Interferon gamma
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Summary:Suppressors of cytokine signaling (SOCS) are proteins that modulate cytokine responses in lymphoid cells. In these studies, cultured primary mouse astrocytes expressed SOCS-3 mRNA constitutively. Treatment with interferon-gamma (IFN-g) induced SOCS-1 and enhanced SOCS-3 expression, and was associated with decreased tumor necrosis factor-alpha (TNF) and increased leukemia inhibitory factor (LIF) in culture supernatants. Treatment with conditioned medium from myelin basic protein-stimulated encephalitogenic lymphoid cells (MBP-CM) increased SOCS-3 and induced SOCS-1 expression. The effects were largely due to IFN-g in MBP-CM, as anti-IFN-g antibody diminished induction. These findings suggest a role for IFN-g-induced SOCS expression in regulation of CNS inflammatory responses by astrocytes.
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ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2004.03.005