Infectious triggers for inflammatory neurological diseases
Nature MedicinePublished 1 May 2002
Kai W. Wucherpfennig
Citations27
SJR quartileQ1
SJR score18.33
SNIP8.71
Generate an AI Snapshot to get a quick, structured summary of this paper.
Study Snapshot
ObjectiveStudy objective
MethodsResearch methodology
PopulationPopulation studied
Sample sizeSample sizes
OutcomesStudy outcomes here
ResultsStudy results comes here
LimitationsResearch study limitations comes here
A concise AI-generated summary of the paper will appear here once you click Generate AI Snapshot.
TL;DR
A new study provides strong evidence for a virus-induced autoimmune process in a human neurological disease.
Abstract
Do autoimmune diseases develop 'spontaneously' or are they induced by environmental triggers, such as infectious agents? This is a central—and challenging—question in the autoimmunity field. A new study in this issue provides strong evidence for a virus-induced autoimmune process in a human neurological disease. ( pages 509–513 )
Keywords
Immunology and MicrobiologyMedicine
CellMolecular mimicry in T cell-mediated autoimmunity: Viral peptides activate human T cell clones specific for myelin basic protein
1,547 Citations1995Kai W. Wucherpfennig, Jack L. Strominger
The observation that a single T cell receptor can recognize quite distinct but structurally related peptides from multiple pathogens has important implications for understanding the pathogenesis of autoimmunity.
ScienceAmino Acid Homology Between the Encephalitogenic Site of Myelin Basic Protein and Virus: Mechanism for Autoimmunity
949 Citations1985Robert S. Fujinami, Michael B. A. Oldstone
Rabbit central nervous system tissue taken from these rabbits had a histologic picture reminiscent of experimental allergic encephalomyelitis, indicating that viral infection may trigger the production of antibodies and mononuclear cells that cross-react with self proteins by a mechanism termed molecular mimicry.
New England Journal of Medicine<i>Campylobacter jejuni</i>Infection and Guillain–Barré Syndrome
758 Citations1995Jeremy Rees, Sara E. Soudain +2 more
Infection with C. jejuni often precedes the Guillain-Barré syndrome and is associated with axonal degeneration, slow recovery, and severe residual disability.
Nature MedicineDiabetes induced by Coxsackie virus: Initiation by bystander damage and not molecular mimicry
668 Citations1998Marc S. Horwitz, Linda M. Bradley +4 more
Results show that diabetes induced by Coxsackie virus infection is a direct result of local infection leading to inflammation, tissue damage, and the release of sequestered islet antigen resulting in the re-stimulation of resting autoreactive T cells, further indicating that the is let antigen sensitization is an indirect consequence of the viral infection.
Proceedings of the National Academy of SciencesHLA alleles determine human T-lymphotropic virus-I (HTLV-I) proviral load and the risk of HTLV-I-associated myelopathy
423 Citations1999Katie Jeffery, Koichiro Usuku +15 more
It is shown that, after infection with HTLV-I, the class I allele HLA-A*02 halves the odds of HAM/TSP, implying that an efficient antiviral CTL response can reduce virus load and so prevent disease in persistent virus infections.
Journal of Clinical InvestigationMechanisms for the induction of autoimmunity by infectious agents
355 Citations2001Kai W. Wucherpfennig
Mechanisms by which an infection can lead to an autoimmune process have been examined in experimental animal models, and these concepts as well as their relevance to human diseases are discussed.
Journal of Clinical InvestigationMechanisms for the induction of autoimmunity by infectious agents
349 Citations2001Kai W. Wucherpfennig
Nature MedicineAutoimmunity due to molecular mimicry as a cause of neurological disease
256 Citations2002Michael C. Levin, Sang Min Lee +8 more
This study establishes a clear link between viral infection, autoimmunity and neurological disease in humans and demonstrates the importance of molecular mimicry between an infecting agent and hnRNP-A1 in autoimmune disease of the CNS.
Journal of Clinical InvestigationA virus-induced molecular mimicry model of multiple sclerosis
204 Citations2001Julie K. Olson, J. Ludovic Croxford +3 more
This is the first study showing that a naturally infectious virus encoding a myelin epitope mimic can directly initiate organ-specific T cell-mediated autoimmunity.
Journal of Clinical InvestigationA virus-induced molecular mimicry model of multiple sclerosis
174 Citations2001Julie K. Olson, J. Ludovic Croxford +3 more
A mouse model of the ability of a virus encoding a self myelin mimic epitope to induce an autoimmune response has been developed and critical information regarding the mechanisms by which infection-induced molecular mimicry can induce autoimmune diseases is provided.
ImmunityAnalysis of the Relationship between Viral Infection and Autoimmune Disease
122 Citations2001Vily Panoutsakopoulou, Marie Sanchirico +6 more
It is indicated that viral mimicry is essential for disease induction after low-level viral infection of animals containing limited numbers of autoreactive T cells, while innate immune mechanisms become sufficient to provoke disease in animals containing relatively high numbers of self-peptide T cells.
The Journal of ImmunologyPeptide Recognition by Two HLA-A2/Tax11–19-Specific T Cell Clones in Relationship to Their MHC/Peptide/TCR Crystal Structures
91 Citations1999Stefan Hausmann, William E. Biddison +6 more
The distinct functional properties of these CTL clones highlight structural features that determine TCR specificity and cross-reactivity for MHC-bound peptides.
Annals of NeurologyNeuronal molecular mimicry in immune‐mediated neurologic disease
69 Citations1998Michael C. Levin, Marc Z. Krichavsky +7 more
It is indicated that HAM/TSP patients develop an antibody response that targets uninfected neurons, yet reactivity is blocked by HTLV‐I, suggesting viral‐specific autoimmune reactivity to the CNS, the damaged target organ in HAM/ TSP.
Current Opinion in NeurologyImmunopathogenesis of human T cell lymphotropic virus type I-associated myelopathy
38 Citations2001Masahiro Nagai, Steven Jacobson
Co-existing high proviral loads and virus-specific CD8 T cells are important features of this disorder, in which a high cellular immune response continuously driven by this virus may contribute to the inflammatory process within central nervous system lesions in patients with this disease.