Faculty

Kouichi Ito
Associate Professor
Department: Department of Neurology
Phone: 1.7322355482
Email: mailto:itoko@rwjms.rutgers.edu
Robert Wood Johnson Medical School
RWJSPH - Room 184
683 Hoes Lane
Piscataway, NJ 08854
Key Words: Multiple Sclerosis, Neuroimmunology, Autoimmune disease, Immune tolerance, Neurodegeneration, Mucosal Immunology

My laboratory focuses on understanding the mechanisms of the development of central nervous system (CNS) autoimmune diseases including Multiple Sclerosis (MS) using MS animal models such as experimental autoimmune encephalomyelitis (EAE). Although autoreactive T cells specific for self-antigens normally undergo tolerance (apoptosis/unresponsiveness), this immune tolerance happens to be broken in autoimmune diseases. In CNS autoimmunity, autoreactive T cells which recognize CNS self-antigens migrate into the CNS and induce inflammation that can trigger the development of neurodegeneration including demyelination and axonal loss. It is still unknown how CNS antigen-specific autoreactive T cells are activated and migrate into the CNS. To investigate the mechanism of how CNS antigen-specific T cells can induce CNS autoimmune disease, we have created humanized transgenic mice that express MS-associated major histocompatibility complex class II HLA-DR genes and CNS antigen-specific T cell receptor genes isolated from MS patients. Interestingly, these humanized transgenic mice develop EAE spontaneously during the young adult period, and this spontaneous EAE development depends on colonization of commensal bacteria in the gut. We are currently investigating the following questions using humanized animal models:

  • How is immune tolerance to CNS antigens broken naturally in spontaneous EAE mice?
  • How does aging affect the development of CNS antigen-specific pathogenic T cells and the induction of CNS autoimmune disease?
  • How does the interaction between the gut immune system and commensal bacteria affect the development of CNS autoimmune disease?
  • How does CNS inflammation trigger neurodegeneration (demyelination and axonal loss)?

Publications