Mechanism of experimental autoimmune encephalomyelitis in Lewis rats

• 발행기관: 대한해부학회
• 저자명: Taekyun Shin Meejung Ahn Yoh Matsumoto
• 간행물 정보: 『Anatomy and Cell Biology』Vol.45(3), 141~148쪽, 전체 8쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2012.09.30

영문 초록

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.

목차

Abstract

Introduction

Encephalitogenic Antigens in Acute EAE in Lewis Rats

Neuropathogenesis of Active EAE in Lewis Rats

Apoptosis of T Cells

Regulatory T Cells

Macrophages

Conclusions and Prospective

Acknowledgements

References

키워드

Experimental autoimmune encephalomyelitis Lewis rats Macrophages Neuroimmunomodulation Regulatory T lymphocytes