ArticleClinical and experimental immunology2016
Intranasal immunization with heat shock protein 60 induces CD4(+) CD25(+) GARP(+) and type 1 regulatory T cells and inhibits early atherosclerosis.
Article in Clinical and experimental immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 41 citations in OpenAlex.
- Chaperonin in health and disease.Molecular biomedicine · 2026Review
- Mitigating atherosclerosis: Integrating vaccines with gene targets.American heart journal plus : cardiology research and practice · 2025Review
- A bibliometric analysis of vaccination against atherosclerosis.Human vaccines & immunotherapeutics · 2024Article
- Vaccination as a Promising Approach in Cardiovascular Risk Mitigation: Are We Ready to Embrace a Vaccine Strategy?Biomolecules · 2024Review
- Overview of multifunctional Tregs in cardiovascular disease: From insights into cellular functions to clinical implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- Atheroprotective Aspects of Heat Shock Proteins.International journal of molecular sciences · 2023Review
- Two decades of vaccine development against atherosclerosis.Nano today · 2023Article
- The role of regulatory T cells and follicular T helper cells in HBV infection.Frontiers in immunology · 2023Review
- Vaccination against Atherosclerosis: Is It Real?International journal of molecular sciences · 2022Review
- GARP as a Therapeutic Target for the Modulation of Regulatory T Cells in Cancer and Autoimmunity.Frontiers in immunology · 2022Review
- ApoB-Specific CD4Cells · 2021Review
- Heat shock protein 60 and cardiovascular diseases: An intricate love-hate story.Medicinal research reviews · 2021Review
- Tolerogenic vaccines for the treatment of cardiovascular diseases.EBioMedicine · 2020Review
- Atheroprotective nasal immunization with a heat shock protein 60 peptide fromJournal of periodontal & implant science · 2020Article
- Elongated Flexuous Plant Virus-Derived Nanoparticles Functionalized for Autoantibody Detection.Nanomaterials (Basel, Switzerland) · 2019Article
- Vaccination against atherosclerosis.Current opinion in immunology · 2019Review
- Getting to the Heart of the Matter: The Role of Regulatory T-Cells (Tregs) in Cardiovascular Disease (CVD) and Atherosclerosis.Frontiers in immunology · 2019Review
- Toward Developing Chemical Modulators of Hsp60 as Potential Therapeutics.Frontiers in molecular biosciences · 2018Review
- Readapting the adaptive immune response - therapeutic strategies for atherosclerosis.British journal of pharmacology · 2017Review
- Vaccine against arteriosclerosis: an update.Therapeutic advances in vaccines · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is an autoimmune inflammatory disease involving both innate and adaptive immune mechanisms. Immune tolerance induction may have therapeutic potential for the suppression of atherosclerosis. Current interest is directed towards mucosal tolerance induction, especially nasal tolerance. Previous studies have shown that heat shock protein 60 (HSP60) is recognized as an important autoantigen in atherosclerosis, and nasal or oral HSP60 can induce tolerance and ameliorate atherosclerosis by inducing several subsets of regulatory T cells (Tregs ) such as latency-associated peptide (LAP)(+) and forkhead box transcription factor 3 (FoxP3)(+) Tregs. However, little is known regarding the detailed mechanisms of nasal tolerance. Here, we again investigated the impact of nasal HSP60 on atherosclerosis and the mechanisms underlying the anti-atherosclerosis responses. We found that nasal HSP60 caused a significant 33·6% reduction in plaque size at the aortic root in the early stages of atherosclerosis (P < 0·001). Notably, a significant increase in activated CD4(+) CD25(+) glycoprotein A repetitions predominant (GARP)(+) Tregs, type 1 Tregs (Tr1 cells), and CD4(+) CD25(+) FoxP3(+) Tregs, as well as a marked decrease in the numbers of type 1 and 17 T helper cells was detected in the spleens and cervical lymph nodes of HSP60-treated mice. Moreover, nasal HSP60 increases the production of transforming growth factor (TGF)-β and interleukin (IL)-10 and decreases the secretion of IFN-γ and IL-17. Interestingly, the atheroprotective role of nasal HSP60 treatment was abrogated partly by the neutralization of IL-10. Our findings show that nasal administration of HSP60 can attenuate atherosclerotic formation by inducing GARP(+) Tregs, Tr1 cells and FoxP3(+) Tregs, and that these Tregs maintain immune homeostasis by secreting IL-10 and TGF-β.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.