ArticleThe Journal of experimental medicine2022
Pathogenic autoantibodies to IFN-γ act through the impedance of receptor assembly and Fc-mediated response.
Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Anti-interferon-γ autoantibodies syndrome and opportunistic infections: systematic literature review.Frontiers in immunology · 2025Pooled it
- Affinity-matured B cell responses neutralizing type-I interferons underlie severe viral infections.Cell · 2026Article
- Toward a monogenic architecture of human infections: From 1996 to 2026.Journal of human immunity · 2026Review
- Identification and characterization of bone marrow plasma cells producing IFN-γ-neutralizing autoantibodies in adult-onset immunodeficiency.Cell reports. Medicine · 2026Article
- Article
- Robust CD8Frontiers in immunology · 2026Article
- A Proteomics Outlook on the Molecular Effectors of CAR-T Cell Therapy in Cancer Management.Journal of proteome research · 2025Review
- Human immunity to fungal infections.The Journal of experimental medicine · 2025Review
- Characteristics of polyclonal anti-interferon-gamma autoantibodies and novel diagnostic strategies: A prospective cohort study of new biomarkers.Journal of translational autoimmunity · 2025Article
- Auto-antibodies against interferons are common in people living with chronic hepatitis B virus infection and associate with PegIFNα non-response.JHEP reports : innovation in hepatology · 2025Article
- Clinical characteristics of acquired anti-IFN-γ autoantibodies in patients infected with non-tuberculous mycobacteria: a prospective cohort study.BMC pulmonary medicine · 2025Article
- A homogeneous bioluminescent inhibition immunoassay to detect anti-interferon gamma antibodies.Clinical and experimental immunology · 2024Article
- Exploring the Contrasts and Similarities of Dengue and SARS-CoV-2 Infections During the COVID-19 Era.International journal of molecular sciences · 2024Review
- Diverse BCR usage and T cell activation induced by different COVID-19 sequential vaccinations.mBio · 2024Article
- A sensitive assay for measuring whole-blood responses to type I IFNs.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Pathogenic Role of Anti-Granulocyte-Macrophage Colony-Stimulating Factor Autoantibodies in the Nocardiosis with the Central Nervous System Involvement.Journal of clinical immunology · 2024Article
- Interferon-Science (New York, N.Y.) · 2024Review
- Anti-cytokine autoantibodies: mechanistic insights and disease associations.Nature reviews. Immunology · 2024Review
- Autoantibodies to Erythropoietin Receptor and Clinical Outcomes in Patients With Type 2 Diabetes and CKD: AKidney international reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
30 authors at 9 institutions in 3 countries.
Funding
Abstract
Anti-interferon (IFN)-γ autoantibodies (AIGAs) are a pathogenic factor in late-onset immunodeficiency with disseminated mycobacterial and other opportunistic infections. AIGAs block IFN-γ function, but their effects on IFN-γ signaling are unknown. Using a single-cell capture method, we isolated 19 IFN-γ-reactive monoclonal antibodies (mAbs) from patients with AIGAs. All displayed high-affinity (KD < 10-9 M) binding to IFN-γ, but only eight neutralized IFN-γ-STAT1 signaling and HLA-DR expression. Signal blockade and binding affinity were correlated and attributed to somatic hypermutations. Cross-competition assays identified three nonoverlapping binding sites (I-III) for AIGAs on IFN-γ. We found that site I mAb neutralized IFN-γ by blocking its binding to IFN-γR1. Site II and III mAbs bound the receptor-bound IFN-γ on the cell surface, abolishing IFN-γR1-IFN-γR2 heterodimerization and preventing downstream signaling. Site III mAbs mediated antibody-dependent cellular cytotoxicity, probably through antibody-IFN-γ complexes on cells. Pathogenic AIGAs underlie mycobacterial infections by the dual blockade of IFN-γ signaling and by eliminating IFN-γ-responsive cells.
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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.