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Multiple sclerosis: are protective immune mechanisms compromised by a complex infectious background?

Bernd Krone¹, John M Grange

¹Institute of Virology, Centre for Hygiene and Human Genetics, University of Göttingen, Kreuzbergring 57, 37075 Göttingen, Germany.

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|January 4, 2011

Summary

Multiple sclerosis (MS) may stem from immune system defects triggered by infections and hygiene, leading to abnormal human endogenous retroviral (HERV) gene expression and impacting CD8(+) T cells crucial for immune repair.

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Area of Science:

Immunology
Neuroimmunology
Infectious Disease Immunology

Background:

Multiple sclerosis (MS) exhibits altered immune responses to infections, notably Epstein-Barr virus.
This immune dysfunction may be a primary driver or a consequence of MS pathogenesis.
Improved hygiene standards potentially lead to immune regulatory defects, affecting responses to endogenous retroviral genes.

Purpose of the Study:

To explore the hypothesis that a complex infectious background and associated immune dysregulation contribute to MS pathogenesis.
To investigate the role of human endogenous retroviral (HERV) gene expression in MS.
To examine the potential impact of impaired CD8(+) T cell function on MS.

Main Methods:

Epidemiological observations were analyzed.
The study discusses immunological mechanisms potentially involved in MS.
Focus on T cell subsets and retroviral gene products.

Main Results:

Altered immune reactivity against infections, particularly Epstein-Barr virus, is a hallmark of MS.
A potential link between improved hygiene, immune regulatory defects, and abnormal HERV gene expression is proposed.
A failure in the expansion or an eclipse of self-antigen-specific CD8(+) T cells, and detrimental HERV gene product activity, are implicated in MS pathogenesis.

Conclusions:

The complex infectious background and subsequent immune dysregulation are key to understanding MS immune pathogenesis.
Defects in immune regulation, possibly linked to hygiene, may permit aberrant HERV gene expression.
Impaired immune repair mediated by CD8(+) T cells and adverse effects of HERV products are suggested as underlying mechanisms in MS.