Interferon-β is a key regulator of proinflammatory events in experimental autoimmune encephalomyelitis
Background: Interferon (IFN)-β is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined. Objectives: Our objective was to characterize the role of IFN-β in immune regulation in experimental autoimmune encephalomyelitis (EAE). Methods: IFN-β...
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Published in | Multiple sclerosis Vol. 16; no. 12; pp. 1458 - 1473 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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London, England
SAGE Publications
01.12.2010
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Abstract | Background: Interferon (IFN)-β is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined.
Objectives: Our objective was to characterize the role of IFN-β in immune regulation in experimental autoimmune encephalomyelitis (EAE).
Methods: IFN-β +/+ and IFN-β—/— mice were immunized with myelin oligodendrocyte glycoprotein peptide in the presence or absence of IFN-β, to induce EAE. Disease pathogenesis was monitored in the context of incidence, time of onset, clinical score, and immune cell activation in the brains, spleens and lymph nodes of affected mice.
Results: Compared with IFN-β+/+ mice, IFN-β—/ — mice exhibited an earlier onset and a more rapid progression of EAE, increased numbers of CD11b+ leukocytes infiltrating affected brains and an increased percentage of Th17 cells in the central nervous system and draining lymph nodes. IFN-β treatment delayed disease onset and reduced disease severity. Ex vivo experiments revealed that the lack of IFN-β results in enhanced generation of autoreactive T cells, a likely consequence of the absence of IFN-β-regulated events in both the CD4+ T cells and antigen-presenting dendritic cells. Gene expression analysis of IFN-β-treated bone marrow macrophages (CD11b +) identified modulation of genes affecting T cell proliferation and Th17 differentiation.
Conclusions: We conclude that IFN-β acts to suppress the generation of autoimmune-inducing Th17 cells during the development of disease as well as modulating pro-inflammatory mediators. |
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AbstractList | Interferon (IFN)-β is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined.
Our objective was to characterize the role of IFN-β in immune regulation in experimental autoimmune encephalomyelitis (EAE).
IFN-β(+/+) and IFN-β(-/-) mice were immunized with myelin oligodendrocyte glycoprotein peptide in the presence or absence of IFN-β, to induce EAE. Disease pathogenesis was monitored in the context of incidence, time of onset, clinical score, and immune cell activation in the brains, spleens and lymph nodes of affected mice.
Compared with IFN-β(+/+) mice, IFN-β(-/-) mice exhibited an earlier onset and a more rapid progression of EAE, increased numbers of CD11b(+) leukocytes infiltrating affected brains and an increased percentage of Th17 cells in the central nervous system and draining lymph nodes. IFN-β treatment delayed disease onset and reduced disease severity. Ex vivo experiments revealed that the lack of IFN-β results in enhanced generation of autoreactive T cells, a likely consequence of the absence of IFN-β-regulated events in both the CD4(+) T cells and antigen-presenting dendritic cells. Gene expression analysis of IFN-β-treated bone marrow macrophages (CD11b(+)) identified modulation of genes affecting T cell proliferation and Th17 differentiation.
We conclude that IFN-β acts to suppress the generation of autoimmune-inducing Th17 cells during the development of disease as well as modulating pro-inflammatory mediators. Background: Interferon (IFN)-β is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined. Objectives: Our objective was to characterize the role of IFN-β in immune regulation in experimental autoimmune encephalomyelitis (EAE). Methods: IFN-β +/+ and IFN-β—/— mice were immunized with myelin oligodendrocyte glycoprotein peptide in the presence or absence of IFN-β, to induce EAE. Disease pathogenesis was monitored in the context of incidence, time of onset, clinical score, and immune cell activation in the brains, spleens and lymph nodes of affected mice. Results: Compared with IFN-β+/+ mice, IFN-β—/ — mice exhibited an earlier onset and a more rapid progression of EAE, increased numbers of CD11b+ leukocytes infiltrating affected brains and an increased percentage of Th17 cells in the central nervous system and draining lymph nodes. IFN-β treatment delayed disease onset and reduced disease severity. Ex vivo experiments revealed that the lack of IFN-β results in enhanced generation of autoreactive T cells, a likely consequence of the absence of IFN-β-regulated events in both the CD4+ T cells and antigen-presenting dendritic cells. Gene expression analysis of IFN-β-treated bone marrow macrophages (CD11b +) identified modulation of genes affecting T cell proliferation and Th17 differentiation. Conclusions: We conclude that IFN-β acts to suppress the generation of autoimmune-inducing Th17 cells during the development of disease as well as modulating pro-inflammatory mediators. Background: Interferon (IFN)-β is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined. Objectives: Our objective was to characterize the role of IFN-β in immune regulation in experimental autoimmune encephalomyelitis (EAE). Methods: IFN-β +/+ and IFN-β —/— mice were immunized with myelin oligodendrocyte glycoprotein peptide in the presence or absence of IFN-β, to induce EAE. Disease pathogenesis was monitored in the context of incidence, time of onset, clinical score, and immune cell activation in the brains, spleens and lymph nodes of affected mice. Results: Compared with IFN-β +/+ mice, IFN-β —/ — mice exhibited an earlier onset and a more rapid progression of EAE, increased numbers of CD11b + leukocytes infiltrating affected brains and an increased percentage of Th17 cells in the central nervous system and draining lymph nodes. IFN-β treatment delayed disease onset and reduced disease severity. Ex vivo experiments revealed that the lack of IFN-β results in enhanced generation of autoreactive T cells, a likely consequence of the absence of IFN-β-regulated events in both the CD4 + T cells and antigen-presenting dendritic cells. Gene expression analysis of IFN-β-treated bone marrow macrophages (CD11b + ) identified modulation of genes affecting T cell proliferation and Th17 differentiation. Conclusions: We conclude that IFN-β acts to suppress the generation of autoimmune-inducing Th17 cells during the development of disease as well as modulating pro-inflammatory mediators. BACKGROUNDInterferon (IFN)-β is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined.OBJECTIVESOur objective was to characterize the role of IFN-β in immune regulation in experimental autoimmune encephalomyelitis (EAE).METHODSIFN-β(+/+) and IFN-β(-/-) mice were immunized with myelin oligodendrocyte glycoprotein peptide in the presence or absence of IFN-β, to induce EAE. Disease pathogenesis was monitored in the context of incidence, time of onset, clinical score, and immune cell activation in the brains, spleens and lymph nodes of affected mice.RESULTSCompared with IFN-β(+/+) mice, IFN-β(-/-) mice exhibited an earlier onset and a more rapid progression of EAE, increased numbers of CD11b(+) leukocytes infiltrating affected brains and an increased percentage of Th17 cells in the central nervous system and draining lymph nodes. IFN-β treatment delayed disease onset and reduced disease severity. Ex vivo experiments revealed that the lack of IFN-β results in enhanced generation of autoreactive T cells, a likely consequence of the absence of IFN-β-regulated events in both the CD4(+) T cells and antigen-presenting dendritic cells. Gene expression analysis of IFN-β-treated bone marrow macrophages (CD11b(+)) identified modulation of genes affecting T cell proliferation and Th17 differentiation.CONCLUSIONSWe conclude that IFN-β acts to suppress the generation of autoimmune-inducing Th17 cells during the development of disease as well as modulating pro-inflammatory mediators. Background: Interferon (IFN)- beta is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined. Objectives: Our objective was to characterize the role of IFN- beta in immune regulation in experimental autoimmune encephalomyelitis (EAE). Methods: IFN- beta +/+ and IFN- beta -/- mice were immunized with myelin oligodendrocyte glycoprotein peptide in the presence or absence of IFN- beta , to induce EAE. Disease pathogenesis was monitored in the context of incidence, time of onset, clinical score, and immune cell activation in the brains, spleens and lymph nodes of affected mice. Results: Compared with IFN- beta +/+ mice, IFN- beta -/ - mice exhibited an earlier onset and a more rapid progression of EAE, increased numbers of CD11b+ leukocytes infiltrating affected brains and an increased percentage of Th17 cells in the central nervous system and draining lymph nodes. IFN- beta treatment delayed disease onset and reduced disease severity. Ex vivo experiments revealed that the lack of IFN- beta results in enhanced generation of autoreactive T cells, a likely consequence of the absence of IFN- beta -regulated events in both the CD4+ T cells and antigen-presenting dendritic cells. Gene expression analysis of IFN- beta -treated bone marrow macrophages (CD11b +) identified modulation of genes affecting T cell proliferation and Th17 differentiation. Conclusions: We conclude that IFN- beta acts to suppress the generation of autoimmune-inducing Th17 cells during the development of disease as well as modulating pro-inflammatory mediators. |
Author | Majchrzak-Kita, B Pennell, LM Murooka, TT Baig, E Fish, EN Galligan, CL Rahbar, R |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20935030$$D View this record in MEDLINE/PubMed |
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Keywords | experimental autoimmune encephalomyelitis (EAE) interferon-β autoimmune disease Th17 multiple sclerosis |
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Snippet | Background: Interferon (IFN)-β is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined.
Objectives:... Interferon (IFN)-β is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined. Our objective was to... Background: Interferon (IFN)-β is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined. Objectives:... BACKGROUNDInterferon (IFN)-β is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined.OBJECTIVESOur... Background: Interferon (IFN)- beta is an effective therapy for relapsing-remitting multiple sclerosis, yet its mechanism of action remains ill-defined.... |
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SubjectTerms | Animals Autoimmunity - immunology Cell Separation Cytokines - biosynthesis Cytokines - immunology Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Female Flow Cytometry Gene Expression Profiling Immunohistochemistry Inflammation - immunology Inflammation - metabolism Inflammation - pathology Interferon-beta - immunology Interferon-beta - metabolism Male Mice Mice, Inbred C57BL Mice, Knockout Th17 Cells - immunology Th17 Cells - metabolism |
Title | Interferon-β is a key regulator of proinflammatory events in experimental autoimmune encephalomyelitis |
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