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Mechanism of experimental autoimmune encephalomyelitis in Lewis rats: recent insights from macrophages.

Shin T, Ahn M, Matsumoto Y - Anat Cell Biol (2012)

Bottom Line: EAE in Lewis rats is induced by encephalitogenic antigens, including myelin basic protein.EAE is mediated by CD4(+) Th1 cells, which secrete pro-inflammatory mediators, and spontaneous recovery is mediated by regulatory T cells.This review will summarize the neuroimmunological aspects of active monophasic EAE, which manifests as neuroinflammation followed by neuroimmunomodulation and/or neuroprotection, with a focus on the role of alternatively activated macrophages.

View Article: PubMed Central - PubMed

Affiliation: Department of Veterinary Anatomy, Veterinary Medical Research Institute, College of Veterinary Medicine, Jeju National University, Jeju, Korea. ; Functional and Systems Neurobiology, Cajal Institute, Madrid, Spain.

ABSTRACT
Experimental autoimmune encephalomyelitis (EAE) in Lewis rats is an acute monophasic paralytic central nervous system disease, in which most rats spontaneously recover from paralysis. EAE in Lewis rats is induced by encephalitogenic antigens, including myelin basic protein. EAE is mediated by CD4(+) Th1 cells, which secrete pro-inflammatory mediators, and spontaneous recovery is mediated by regulatory T cells. Recently, it was established that classically activated macrophages (M1 phenotype) play an important role in the initiation of EAE, while alternatively activated macrophages (M2 phenotype) contribute to spontaneous recovery from rat EAE. This review will summarize the neuroimmunological aspects of active monophasic EAE, which manifests as neuroinflammation followed by neuroimmunomodulation and/or neuroprotection, with a focus on the role of alternatively activated macrophages.

No MeSH data available.


Related in: MedlinePlus

Schematic diagram of the putative role of each macrophage phenotype in active monophasic experimental autoimmune encephalomyelitis (EAE) in Lewis rats. EAE is mediated by CD4+ Th1 cells and is further accelerated by classically activated macrophages (M1), while spontaneous recovery from rat EAE is associated with regulatory T cells and alternatively activated macrophages (M2). IFN, interferon; IL, interleukin; iNOS, inducible nitric oxide synthase; TGF, transforming growth factor; TNF, tumor necrosis factor.
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Figure 1: Schematic diagram of the putative role of each macrophage phenotype in active monophasic experimental autoimmune encephalomyelitis (EAE) in Lewis rats. EAE is mediated by CD4+ Th1 cells and is further accelerated by classically activated macrophages (M1), while spontaneous recovery from rat EAE is associated with regulatory T cells and alternatively activated macrophages (M2). IFN, interferon; IL, interleukin; iNOS, inducible nitric oxide synthase; TGF, transforming growth factor; TNF, tumor necrosis factor.

Mentions: Macrophages are regarded as an important cell type at the induction stage of rat EAE [32, 33], because blocking of macrophages ameliorated the condition. In addition, increased numbers of macrophages have been associated with the severity of rat acute EAE [22], and macrophages are associated with increased expression of pro-inflammatory mediators, including TNF-alpha and inducible nitric oxide synthase (iNOS) [22]. Macrophages that express TNF-alpha and/or iNOS are classified as classically activated macrophages, or M1 phenotype cells (Fig. 1).


Mechanism of experimental autoimmune encephalomyelitis in Lewis rats: recent insights from macrophages.

Shin T, Ahn M, Matsumoto Y - Anat Cell Biol (2012)

Schematic diagram of the putative role of each macrophage phenotype in active monophasic experimental autoimmune encephalomyelitis (EAE) in Lewis rats. EAE is mediated by CD4+ Th1 cells and is further accelerated by classically activated macrophages (M1), while spontaneous recovery from rat EAE is associated with regulatory T cells and alternatively activated macrophages (M2). IFN, interferon; IL, interleukin; iNOS, inducible nitric oxide synthase; TGF, transforming growth factor; TNF, tumor necrosis factor.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3472139&req=5

Figure 1: Schematic diagram of the putative role of each macrophage phenotype in active monophasic experimental autoimmune encephalomyelitis (EAE) in Lewis rats. EAE is mediated by CD4+ Th1 cells and is further accelerated by classically activated macrophages (M1), while spontaneous recovery from rat EAE is associated with regulatory T cells and alternatively activated macrophages (M2). IFN, interferon; IL, interleukin; iNOS, inducible nitric oxide synthase; TGF, transforming growth factor; TNF, tumor necrosis factor.
Mentions: Macrophages are regarded as an important cell type at the induction stage of rat EAE [32, 33], because blocking of macrophages ameliorated the condition. In addition, increased numbers of macrophages have been associated with the severity of rat acute EAE [22], and macrophages are associated with increased expression of pro-inflammatory mediators, including TNF-alpha and inducible nitric oxide synthase (iNOS) [22]. Macrophages that express TNF-alpha and/or iNOS are classified as classically activated macrophages, or M1 phenotype cells (Fig. 1).

Bottom Line: EAE in Lewis rats is induced by encephalitogenic antigens, including myelin basic protein.EAE is mediated by CD4(+) Th1 cells, which secrete pro-inflammatory mediators, and spontaneous recovery is mediated by regulatory T cells.This review will summarize the neuroimmunological aspects of active monophasic EAE, which manifests as neuroinflammation followed by neuroimmunomodulation and/or neuroprotection, with a focus on the role of alternatively activated macrophages.

View Article: PubMed Central - PubMed

Affiliation: Department of Veterinary Anatomy, Veterinary Medical Research Institute, College of Veterinary Medicine, Jeju National University, Jeju, Korea. ; Functional and Systems Neurobiology, Cajal Institute, Madrid, Spain.

ABSTRACT
Experimental autoimmune encephalomyelitis (EAE) in Lewis rats is an acute monophasic paralytic central nervous system disease, in which most rats spontaneously recover from paralysis. EAE in Lewis rats is induced by encephalitogenic antigens, including myelin basic protein. EAE is mediated by CD4(+) Th1 cells, which secrete pro-inflammatory mediators, and spontaneous recovery is mediated by regulatory T cells. Recently, it was established that classically activated macrophages (M1 phenotype) play an important role in the initiation of EAE, while alternatively activated macrophages (M2 phenotype) contribute to spontaneous recovery from rat EAE. This review will summarize the neuroimmunological aspects of active monophasic EAE, which manifests as neuroinflammation followed by neuroimmunomodulation and/or neuroprotection, with a focus on the role of alternatively activated macrophages.

No MeSH data available.


Related in: MedlinePlus