Mechanism of experimental autoimmune neuritis in Lewis rats: the dual role of macrophages
Taekyun Shin1,2, Meejung Ahn3, Yoh Matsumoto4 and Changjong Moon5
1Department of Veterinary Anatomy, College of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju, Republic of Korea 2Functional and Systems Neurobiology, Cajal Institute, Madrid, Spain, 3Department of Anatomy, College of Medicine, Jeju National University, Jeju, Republic of Korea, 4Department of Immunotherapy Development, Tokyo Metropolitan Institute of Medical Science, Kamikitazawa, Setagayaku, Tokyo, Japan and 5Department of Veterinary Anatomy, College of Veterinary Medicine and Animal Medical Institute, Chonnam National University, Gwangju, Republic of Korea.
Offprint requests to: Taekyun Shin, Department of Veterinary Anatomy, College of Veterinary Medicine, Jeju National University, Jeju 690-756, Republic of Korea. e-mail: firstname.lastname@example.org, or Changjong Moon, e-mail: email@example.com.
Summary. Human peripheral demyelinating diseases, such as Guillain-Barré syndrome (GBS), are characterized by inflammation and demyelination in the peripheral nervous system. Similarities in the pathology between GBS and the animal model of experimental autoimmune neuritis (EAN) indicate that autoimmune responses are involved in both diseases. This article summarizes the general aspects of the EAN model in Lewis rats and discusses the potential role of macrophages in the progression of EAN. A better understanding of macrophages may help to design alternative therapeutic strategies for organ-specific autoimmune diseases, including GBS. Histol Histopathol 28, 679-684 (2013)
Key words: Alternatively activated macrophages, Experimental autoimmune neuritis, Guillain-Barré syndrome, Peripheral nervous system inflammation