ArticleProceedings of the National Academy of Sciences of the United States of America2014
Monoclonal antibody blocking the recognition of an insulin peptide-MHC complex modulates type 1 diabetes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 62 citations in OpenAlex.
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- Antigen-specific modulation of chronic experimental autoimmune encephalomyelitis in humanized mice by TCR-like antibody targeting autoreactive T-cell epitope.Life science alliance · 2025Article
- Antigen-specific T cell responses in autoimmune diabetes.Frontiers in immunology · 2024Review
- Regulatory T cells targeting a pathogenic MHC class II: Insulin peptide epitope postpone spontaneous autoimmune diabetes.Frontiers in immunology · 2023Article
- Alternative CAR Therapies: Recent Approaches in Engineering Chimeric Antigen Receptor Immune Cells to Combat Cancer.Biomedicines · 2022Review
- A Novel Tolerogenic Antibody Targeting Disulfide-Modified Autoantigen Effectively Prevents Type 1 Diabetes in NOD Mice.Frontiers in immunology · 2022Article
- TCR-like antibodies targeting autoantigen-mhc complexes: a mini-review.Frontiers in immunology · 2022Review
- Cell-based therapies for rheumatoid arthritis: opportunities and challenges.Therapeutic advances in musculoskeletal disease · 2022Review
- A high-affinity human TCR-like antibody detects celiac disease gluten peptide-MHC complexes and inhibits T cell activation.Science immunology · 2021Article
- Therapeutic Advances in Diabetes, Autoimmune, and Neurological Diseases.International journal of molecular sciences · 2021Review
- Auto-antigen and Immunomodulatory Agent-Based Approaches for Antigen-Specific Tolerance in NOD Mice.Current diabetes reports · 2021Review
- Therapeutic Targeting of Autoreactive B Cells: Why, How, and When?Biomedicines · 2021Review
- Emerging Therapeutics for Immune Tolerance: Tolerogenic Vaccines, T cell Therapy, and IL-2 Therapy.Frontiers in immunology · 2021Review
- Proinsulin-Reactive CD4 T Cells in the Islets of Type 1 Diabetes Organ Donors.Frontiers in endocrinology · 2021Article
- Retro-inverso D-peptides as a novel targeted immunotherapy for Type 1 diabetes.Journal of autoimmunity · 2020Article
- Type 1 diabetes pathogenesis and the role of inhibitory receptors in islet tolerance.Annals of the New York Academy of Sciences · 2020Review
- Peptide mimotopes alter T cell function in cancer and autoimmunity.Seminars in immunology · 2020Review
- Immune therapies for autoimmune diabetes targeting pathogenic peptide-MHC complexes.Journal of molecular cell biology · 2020Review
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
The primary autoantigen triggering spontaneous type 1 diabetes mellitus in nonobese diabetic (NOD) mice is insulin. The major T-cell insulin epitope lies within the amino acid 9-23 peptide of the β-chain (B:9-23). This peptide can bind within the peptide binding groove of the NOD MHC class II molecule (MHCII), IA(g7), in multiple positions or "registers." However, the majority of pathogenic CD4 T cells recognize this complex only when the insulin peptide is bound in register 3 (R3). We hypothesized that antibodies reacting specifically with R3 insulin-IA(g7) complexes would inhibit autoimmune diabetes specifically without interfering with recognition of other IA(g7)-presented antigens. To test this hypothesis, we generated a monoclonal antibody (mAb287), which selectively binds to B:9-23 and related variants when presented by IA(g7) in R3, but not other registers. The monoclonal antibody blocks binding of IA(g7)-B:10-23 R3 tetramers to cognate T cells and inhibits T-cell responses to soluble B:9-23 peptides and NOD islets. However, mAb287 has no effect on recognition of other peptides bound to IA(g7) or other MHCII molecules. Intervention with mAb287, but not irrelevant isotype matched antibody, at either early or late stages of disease development, significantly delayed diabetes onset by inhibiting infiltration by not only insulin-specific CD4 T cells, but also by CD4 and CD8 T cells of other specificities. We propose that peptide-MHC-specific monoclonal antibodies can modulate autoimmune disease without the pleiotropic effects of nonselective reagents and, thus, could be applicable to the treatment of multiple T-cell mediated autoimmune disorders.
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