ArticleJournal of autoimmunity2013
Hsp65-producing Lactococcus lactis prevents experimental autoimmune encephalomyelitis in mice by inducing CD4+LAP+ regulatory T cells.
Article in Journal of autoimmunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Pooled it
- Oral GAD65-Microorganisms · 2026Article
- Article
- Lactococcus lactis-HSP65 requires TLR2 to induce tolerogenic dendritic cells and confer protection against type 1 diabetes in a murine model.Cellular and molecular life sciences : CMLS · 2025Article
- Engineering the Microbiome: a Novel Approach to Managing Autoimmune Diseases.Neuromolecular medicine · 2025Review
- Metagenomic and metabolomic analysis of gut microbiome's role in spinal cord injury recovery in rats.Biomolecules & biomedicine · 2025Article
- Gut microbiota and other factors associated with increased T cell regulation in HIV-exposed uninfected infants.Frontiers in immunology · 2025Article
- The link between gut microbiota and multiple sclerosis from the perspective of barrier function.Frontiers in immunology · 2025Review
- Relationship between gut microbiota and multiple sclerosis: a scientometric visual analysis from 2010 to 2023.Frontiers in immunology · 2024Article
- Remyelination in multiple sclerosis, along with its immunology and association with gut dysbiosis, lifestyle, and environmental factors.Annals of medicine and surgery (2012) · 2023Review
- The Molecular Role of Immune Cells in Dilated Cardiomyopathy.Medicina (Kaunas, Lithuania) · 2023Review
- The role of the gut microbiota in multiple sclerosis.Nature reviews. Neurology · 2022Review
- Intake ofMicroorganisms · 2021Article
- ILC3, a Central Innate Immune Component of the Gut-Brain Axis in Multiple Sclerosis.Frontiers in immunology · 2021Review
- Oral tolerance as antigen-specific immunotherapy.Immunotherapy advances · 2021Review
- Oral Tolerance Induced by Heat Shock Protein 65-ProducingFrontiers in immunology · 2021Article
- Immunoregulatory Effects of Tolerogenic Probiotics in Multiple Sclerosis.Advances in experimental medicine and biology · 2021Review
- Modulating Gut Microbiota: An Emerging Approach in the Prevention and Treatment of Multiple Sclerosis.Current neuropharmacology · 2021Review
- Engineering the gut microbiota to treat chronic diseases.Applied microbiology and biotechnology · 2020Review
- The Microbiome as a Therapeutic Target for Multiple Sclerosis: Can Genetically Engineered Probiotics Treat the Disease?Diseases (Basel, Switzerland) · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Heat shock proteins (Hsps) participate in the cellular response to stress and they are hiperexpressed in inflammatory conditions. They are also known to play a major role in immune modulation, controlling, for instance, autoimmune responses. In this study, we showed that oral administration of a recombinant Lactococcus lactis strain that produces and releases LPS-free Hsp65 prevented the development of experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice. This was confirmed by the reduced inflammatory cell infiltrate and absence of injury signs in the spinal cord. The effect was associated with reduced IL-17 and increased IL-10 production in mesenteric lymph node and spleen cell cultures. Hsp65-producing-L. lactis-fed mice had a remarkable increase in the number of natural and inducible CD4+Foxp3+ regulatory T (Treg) cells and CD4+LAP+ (Latency-associated peptide) Tregs - which express the membrane-bound TGF-β - in spleen, inguinal and mesenteric lymph nodes as well as in spinal cord. Moreover, many Tregs co-expressed Foxp3 and LAP. In vivo depletion of LAP+ cells abrogated the effect of Hsp65-producing L. lactis in EAE prevention and worsened disease in medium-fed mice. Thus, Hsp65-L.lactis seems to boost this critical regulatory circuit involved in controlling EAE development in mice.
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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.