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Subject: MHC

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    Book Part
    Citation - Scopus: 2
    Molecular Mimicry Study Between Peptides of SARS-CoV-2 and Neutrophil Extracellular Traps-Related Proteins
    (Elsevier, 2024) Adiguzel,Y.; Shoenfeld,Y.
    Background Neutrophil extracellular traps (NETs) are observed in both COVID-19 pathology and autoimmune disorders, and molecular mimicry is a mechanism that can lead to an autoimmune response. Methods Similar sequences between SARS-CoV-2 proteins and 5 proteins (plasminogen receptor KT: PLRKT, myeloperoxidase: MPO, proteinase 3: PR-3, neutrophil elastase: NE, matrix metalloproteinase 9: MMP-9) that are present in NETs were searched. Human and SARS-CoV-2 sequence pairs were identified. Those among the identified sequence pairs, which are predicted as strong-binding peptides or epitopes of the same selected MHC class I and class II alleles, were predicted. Results In the case of MHC class I alleles, similar PLRKT and SARS-CoV-2 peptide sequences with high predicted-affinities to HLA-A*24:02, HLA-B*08:01, and HLA-B*15:01; similar MPO and SARS-CoV-2 peptide sequences with strong predicted-affinities to HLA-A*01:01, HLA-A*26:01, and HLA-B*15:01; and similar MMP-9 and SARS-CoV-2 peptide sequences with elevated predicted-affinities to HLA-B*39:01 were predicted. In the case of MHC class II alleles, similar PLRKT and SARS-CoV-2 peptide sequences with high predicted-affinities to HLA-DPA1*02:01/DPB1*01:01 were predicted. Conclusion This work is a proof-of-concept study, which revealed the potential involvement of molecular mimicry in NET pathology within susceptible individuals, in the case of being infected with SARS-CoV-2, leading to autoimmunity. © 2024 Elsevier B.V. All rights reserved.
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    Book Part
    Perspectives on Molecular Mimicry Between Human, Sars-Cov and Plasmodium Species Through a Probabilistic and Evolutionary Insight
    (Elsevier, 2024) Adiguzel,Y.; Shoenfeld,Y.
    This chapter examines potential molecular mimicry between similar peptide sequences and shared 6mers of five selected proteins and the proteomes of both SARS-CoV-2 and five Plasmodium species that infect humans (P. falciparum, P. malariae, P. vivax, P. knowlesi, and P. ovale). Human proteins are plasminogen receptor (KT), neutrophil collagenase (neutrophil collagenase isoform 2), myeloperoxidase precursor, mitochondrial peptide methionine sulfoxide reductase isoform a precursor, and myeloblastin precursor. The chapter eventually focuses on a probabilistic and evolutionary insight into molecular mimicry. © 2024 Elsevier B.V. All rights reserved.
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    Review
    Citation - WoS: 6
    Citation - Scopus: 6
    Shared Pathogenicity Features and Sequences Between Ebv, Sars-Cov and Hla Class I Molecule-Binding Motifs With a Potential Role in Autoimmunity
    (Humana Press inc, 2023) Adiguzel, Yekbun; Mahroum, Naim; Muller, Sylviane; Blank, Miri; Halpert, Gilad; Shoenfeld, Yehuda
    Epstein-Barr virus (EBV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are extraordinary in their ability to activate autoimmunity as well as to induce diverse autoimmune diseases. Here we reviewed the current knowledge on their relation. Further, we suggested that molecular mimicry could be a possible common mechanism of autoimmunity induction in the susceptible individuals infected with SARS-CoV-2. Molecular mimicry between SARS-CoV-2 and human proteins, and EBV and human proteins, are present. Besides, relation of the pathogenicity associated with both coronavirus diseases and EBV supports the notion. As a proof-of-the-concept, we investigated 8mer sequences with shared 5mers of SARS-CoV-2, EBV, and human proteins, which were predicted as epitopes binding to the same human leukocyte antigen (HLA) supertype representatives. We identified significant number of human peptide sequences with predicted-affinities to the HLA-A*02:01 allele. Rest of the peptide sequences had predicted-affinities to the HLA-A*02:01, HLA-B*40:01, HLA-B*27:05, HLA-A*01:01, and HLA-B*39:01 alleles. Carriers of these serotypes can be under a higher risk of autoimmune response induction upon getting infected, through molecular mimicry-based mechanisms common to SARS-CoV-2 and EBV infections. We additionally reviewed established associations of the identified proteins with the EBV-related pathogenicity and with the autoimmune diseases.