ReviewJournal of neurovirology2002
Autoimmunity as the body's defense mechanism against the enemy within: Development of therapeutic vaccines for neurodegenerative disorders.
Review in Journal of neurovirology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 9 citations in OpenAlex.
- HMGB1 acts on microglia Mac1 to mediate chronic neuroinflammation that drives progressive neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Neural immunity: Friend or foe?Journal of neurovirology · 2002Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insults to the central nervous system (CNS), whether of microbial or microbe-free origin, result in tissue damage. Until recently, it was generally believed that only microbe-related damage elicits an adaptive immune response, the purpose of which is to eliminate the offending microorganisms. Recent studies in the author's laboratory suggest, however, that the body exhibits an adaptive immune response to microbe-free injuries as well. The immune response in this case is directed against dominant self-antigens residing in the damaged site, where such an adaptive anti-self immune response reinforces the protective activity of local resident cells by providing them with factors that can augment and regulate their capacity for buffering troublemakers such as destructive self-compounds emerging from the injured neural tissue. Because the specificity of this autoimmune response apparently depends not on the type but on the site of lesion, the response can be boosted by therapeutic vaccination for acute and chronic neurodegenerative conditions irrespective of their primary etiology. The results have far-reaching implications, both for microbial infections and for neurodegenerative diseases of the CNS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.