Related Experiment Videos
Anti-adhesion molecule therapy in experimental autoimmune encephalomyelitis
B Cannella1, A H Cross, C S Raine
1Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, NY 10461.
Journal of Neuroimmunology
|July 1, 1993
Summary
Monoclonal antibodies targeting intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) did not significantly prevent experimental allergic encephalomyelitis (EAE) in mice. However, the study suggests these antibodies may have opposing effects on EAE development.
Area of Science:
- Neuroimmunology
- Molecular Immunology
Background:
- Inflammatory episodes in the central nervous system (CNS) correlate with increased adhesion molecules around blood vessels.
- Experimental allergic encephalomyelitis (EAE) is a model for CNS inflammation.
Purpose of the Study:
- To investigate the efficacy of blocking adhesion molecules ICAM-1 and LFA-1 in preventing EAE.
- To explore the potential of monoclonal antibodies (mAbs) against ICAM-1 and LFA-1 in treating EAE.
Main Methods:
- Adoptive transfer of myelin basic protein-specific lymphocytes to induce EAE in SJL/J mice.
- Administration of anti-ICAM-1 and anti-LFA-1 mAbs at varying doses and time points.
- Monitoring EAE development and assessing adhesion molecule expression in the CNS.
Main Results:
- Neither anti-ICAM-1 nor anti-LFA-1 mAbs significantly altered the overall outcome of EAE.
- Adverse effects were observed in some mice treated with anti-LFA-1.
- Down-regulation of targeted adhesion molecules in the CNS was noted post-treatment.
Conclusions:
- Blocking ICAM-1 and LFA-1 with mAbs did not prevent EAE in this murine model.
- The study suggests potential opposing roles for ICAM-1 and LFA-1 in EAE, possibly due to LFA-1's involvement in cell signaling.
- Further research is needed to determine if treatment timing influences therapeutic effects.