ArticlePloS one2025
Immuno-informatics voyage through molecular mimicry of Heat Shock Proteins: Potential IBD immunopathogenesis.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- In silico design of a multi-epitope vaccine against the triple negative breast cancer.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe interplay between the gut microbiota axis and host immunity is pivotal in the pathogenesis of inflammatory bowel disease (IBD), an idiopathic inflammatory condition. Molecular mimicry may be at the root of autoimmune and auto-inflammatory diseases, such as IBD, when microbial antigens and host proteins share structural and molecular similarities. However, auto-inflammation can also occur through mechanisms independent of molecular mimicry. The present study focused on the possible involvement of intestinal bacterial heat shock proteins (HSPs) in the immunopathogenesis of IBD as a cutting-edge issue.
methodsWe employed an immuno-informatics approach to evaluate host-microbe interactions and predict the involvement of bacterial HSPs 60, 70, and 90 in IBD via molecular mimicry as our primary objective. The substantial evolutionary conservation of HSPs and their presence in inflammation scenarios propelled our research. To validate our approach, we performed docking and molecular dynamics (MD) simulations on selected HLA-epitope complexes.
resultsOur analysis revealed that all studied bacteria, compared to Homo sapiens, exhibited meaningful sequence similarity and identity of HSPs. Thirteen bacterial species and their corresponding thirteen epitopes derived from HSP counterparts were selected for further investigation. Finally, a specific epitope of human HSP60 and three epitopes of HSP70 demonstrated considerable sequence similarity to their bacterial counterparts, which was further corroborated through MD simulations as a primary outcome. The secondary outcomes encompassed various factors, including assessing residues in the epitope and receptor-binding grooves within the epitope-HLA complex. Based on the secondary data analysis, the co-expression findings suggested that HSP70 could serve as epitopes in eliciting T-cell-mediated autoimmune responses during infections.
conclusionThe study provided evidence of molecular mimicry between microbial and human HSPs, which could serve as molecular targets for cross-reactive T cells. In addition to considering sequence similarity, our study emphasized the importance of structural interactions as essential factors in cell signaling and immunological pathways.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.