Related Experiment Videos
Pathogenesis of multiple sclerosis: an update on immunology
Bernhard Hemmer1, Sabine Cepok, Stefan Nessler
1Department of Neurology, Philipps University, Rudolf Bultmann Strasse 8, 35033 Marburg, Germany. hemmer@mailer.uni-marburg.de
Current Opinion in Neurology
|June 5, 2002
Summary
Multiple sclerosis involves central nervous system inflammation. Recent findings challenge the T helper type 1 cell theory, revealing diverse immune cells contribute to multiple sclerosis and experimental autoimmune encephalomyelitis pathogenesis.
Area of Science:
- Neuroimmunology
- Autoimmune Disorders
Background:
- Multiple sclerosis (MS) is a central nervous system demyelinating disease.
- MS pathogenesis was historically attributed to myelin-specific CD4 T helper type 1 cells and tumor necrosis factor alpha.
- This paradigm guided early therapeutic strategies.
Purpose of the Study:
- To review recent advancements in understanding MS and experimental autoimmune encephalomyelitis (EAE) pathogenesis.
- To discuss the evolving role of various immune cells beyond the T helper type 1 paradigm.
- To explore implications for novel therapeutic strategies in MS.
Main Methods:
- Review of current literature on experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS).
- Analysis of recent findings on immune cell involvement in central nervous system inflammation.
- Synthesis of data to re-evaluate established pathogenetic models.
Main Results:
- Evidence suggests a more complex immune response in MS and EAE than previously thought.
- Multiple immune cell types, not solely CD4 T helper type 1 cells, are implicated in disease development.
- Tumor necrosis factor alpha's role is being re-examined within this broader context.
Conclusions:
- The simplistic CD4 T helper type 1 cell model for MS is insufficient.
- A multifactorial immune approach is necessary for understanding MS pathogenesis.
- New therapeutic strategies should consider the diverse immune players involved in multiple sclerosis.