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Updated: Jun 11, 2026

Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis
Published on: December 1, 2023
Viral triggers of multiple sclerosis
Kristina Kakalacheva1, Christian Münz, Jan D Lünemann
1Institute of Experimental Immunology, University of Zurich, Switzerland.
Abstract:
Genetic and environmental factors jointly determine the susceptibility to develop Multiple Sclerosis (MS). Collaborative efforts during the past years achieved substantial progress in defining the genetic architecture, underlying susceptibility to MS. Similar to other autoimmune diseases, HLA-DR and HLA-DQ alleles within the HLA class II region on chromosome 6p21 are the highest-risk-conferring genes. Less-robust susceptibility effects have been identified for MHC class I alleles and for non-MHC regions. The role of environmental risk factors and their interaction with genetic susceptibility alleles are much less well defined, despite the fact that infections have long been associated with MS development. Current data suggest that infectious triggers are most likely ubiquitous, i.e., highly prevalent in the general population, and that they require a permissive genetic trait which predisposes for MS development. In this review article, we illustrate mechanisms of infection-induced immunopathologies in experimental animal models of autoimmune CNS inflammation, discuss challenges for the translation of these experimental data into human immunology research, and provide future perspectives on how novel model systems could be utilized to better define the role of viral pathogens in MS.
Insights
Genetic and environmental factors influence Multiple Sclerosis (MS) risk. This review explores infection-induced immunopathologies in animal models and discusses translating these findings to human research for better understanding MS.
Area of Science:
- Immunology
- Neuroscience
- Genetics
Background:
- Multiple Sclerosis (MS) susceptibility is influenced by both genetic and environmental factors.
- Major genetic risk factors include HLA class II alleles, with less robust associations for MHC class I and non-MHC regions.
- The interplay between environmental triggers, particularly infections, and genetic predisposition in MS remains incompletely understood.
Purpose of the Study:
- To review mechanisms of infection-induced immunopathologies in experimental autoimmune central nervous system (CNS) inflammation.
- To discuss challenges in translating findings from animal models to human immunology research for MS.
- To propose future directions using novel model systems to elucidate the role of viral pathogens in MS.
Main Methods:
- Review of existing literature on genetic and environmental factors in MS.
- Analysis of experimental animal models of autoimmune CNS inflammation.
- Discussion of translational challenges and future research perspectives.
Main Results:
- HLA class II alleles are the strongest genetic risk factors for MS.
- Infectious triggers are likely common, requiring a permissive genetic background for MS development.
- Experimental models demonstrate infection-induced immunopathologies relevant to CNS autoimmunity.
Conclusions:
- Understanding the interaction between ubiquitous infectious agents and genetic susceptibility is crucial for MS pathogenesis.
- Bridging the gap between animal models and human MS research is essential.
- Novel model systems are needed to precisely define the role of viral infections in MS development.
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