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Cited by 183Streptococcal Infections and TreatmentsViral Infections and Immunology ResearchSystemic Lupus Erythematosus Research

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Mimicry in Recognition of Cardiac Myosin Peptides by Heart-Intralesional T Cell Clones from Rheumatic Heart Disease

Faé, Kellen C, da Silva, Danielle Diefenbach, Oshiro, Sandra E, Tanaka, Ana C, Pomerantzeff, Pablo M A, Douay, Corinne, Charron, Dominique, Toubert, Antoine, Cunningham, Madeleine W, Kalil, Jorge, Guilherme, Luiza·2006·The Journal of Immunology
DOI 10.4049/jimmunol.176.9.5662
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Abstract

Molecular mimicry between Streptococcus pyogenes Ags and human proteins has been considered as a mechanism leading to autoimmune reactions in rheumatic fever and rheumatic heart disease (RHD). Cardiac myosin has been shown as a putative autoantigen recognized by autoantibodies of rheumatic fever patients. We assessed the human heart-intralesional T cell response against human light meromyosin (LMM) and streptococcal M5 peptides and mitral-valve-derived proteins by proliferation assay. Cytokines induced by LMM peptides were also evaluated. The frequency of intralesional T cell clones that recognized LMM peptides was 63.2%. Thirty-four percent of T cell clones presented cross-reactivity with different patterns: 1) myosin and valve-derived proteins; 2) myosin and streptococcal M5 peptides; and 3) myosin, valve-derived proteins and M5 peptides. In addition, several LMM peptides were recognized simultaneously showing a multiple reactivity pattern of heart-infiltrating T cells. Inflammatory cytokines (IFN-γ and TNF-α) were predominantly produced by heart-infiltrating T cells upon stimulation with LMM peptides. The alignment of LMM and streptococcal M5 peptides showed frequent homology among conserved amino acid substitutions. This is the first study showing the cellular response by human heart-infiltrating T cells against cardiac myosin epitopes in RHD patients. The high percentage of reactivity against cardiac myosin strengthens its role as one of the major autoantigens involved in rheumatic heart lesions. T cell reactivity toward myosin epitopes in RHD patients may also trigger the broad recognition of valvular proteins with structural or functional similarities.

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  • A high homology exists between the M protein expressed in group A Streptococci, the causative microbes of rheumatic heart disease, and the β-MyHC isoform.

    “A study has reported a high homology between the M protein expressed in group A Streptococci , the causative microbes of rheumatic heart disease, and the β -MyHC isoform. 284”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [284]

  • Heart T cells isolated from patients with rheumatic heart disease are activated in the presence of β-MyHC peptides in vitro.

    “In this study, heart T cells isolated from patients with rheumatic heart disease were found to be activated in the presence of β -MyHC peptides in vitro. 284”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [284]

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Metadata

Authors
Faé, K. C., da Silva, D. D., Oshiro, S. E., Tanaka, A. C., Pomerantzeff, P. M. A., Douay, C., Charron, D., Toubert, A., Cunningham, M. W., Kalil, J., & Guilherme, L.
Affiliations
  • Heart Institute (Instituto do Coração) University of São Paulo, School of Medicine , São Paulo ,
  • Universidade de São Paulo (BR)
  • Inserm (FR)
  • University of Oklahoma Health Sciences Center (US)
Corresponding author
  • Kalil, Jorge
  • Guilherme, Luiza
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2006-05-01
Volume
176
Issue
9
Pages
5662-5670
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.176.9.5662
OpenAlex
W1607131709
Cited by
183
References
50
Citations by year
2026: 9 · 2025: 8 · 2024: 10 · 2023: 12 · 2022: 7 · 2021: 5 · 2020: 5 · 2019: 10 · 2018: 6 · 2017: 8 · 2016: 12 · 2015: 6 · 2014: 11 · 2013: 13 · 2012: 13
FWCI
9.36
Type
journal article
Language
en
Open access
closed
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Heart, Lung, and Blood Institute (R56HL056267, R01HL056267, R37HL035280, HL-56267, HL35280)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Streptococcal Infections and Treatments
  • Health Sciences › Medicine › Infectious Diseases › Viral Infections and Immunology Research
  • Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
Keywords
rheumatic heart disease, cardiac myosin, light meromyosin, molecular mimicry, Streptococcus pyogenes, autoantigens, T cell cross-reactivity, rheumatic fever, autoimmunity, interferon-gamma, TNF-α, cytokine production, T cell clones
MeSH terms
Amino Acid Sequence, Bacterial Proteins, Cell Line, Clone Cells, Cross Reactions, Humans, Molecular Sequence Data, Peptide Fragments, Rheumatic Heart Disease, T-Lymphocytes, Myosin Subfragments, Cytokines, Sequence Homology, Amino Acid, Molecular Mimicry, Inflammation Mediators, Epitopes, T-Lymphocyte, Cardiac Myosins

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