ArticleThe Journal of allergy and clinical immunology2016
Expansion of inflammatory innate lymphoid cells in patients with common variable immune deficiency.
Article in The Journal of allergy and clinical immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 87 citations in OpenAlex.
- Beyond B cells: T and Innate Immune Mechanisms of Autoimmunity in Common Variable Immunodeficiency.Clinical reviews in allergy & immunology · 2026Review
- Nodular lymphoid hyperplasia in atypical SCID due to IL7R mutations mimicking CVID.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026Article
- IgA defects in CVID lead to bacterial translocation, increased serum γ-interferon, and BAFF.Journal of human immunity · 2026Article
- Association Between Common Variable Immunodeficiency and Pulmonary Amyloidosis: Review.Journal of clinical medicine · 2026Review
- Multifaceted Roles of IL-26 in Physiological and Pathological Conditions.International journal of molecular sciences · 2025Review
- IL-26 from innate lymphoid cells regulates early-life gut epithelial homeostasis by shaping microbiota composition.The EMBO journal · 2025Article
- Phantom of the immunologic opera: Unmasking the role of innate lymphoid cells (ILC) in inborn errors of immunity (IEI).Journal of human immunity · 2025Review
- Common variable immunodeficiency: autoimmune cytopenias and advances in molecular diagnosis.Hematology. American Society of Hematology. Education Program · 2024Review
- Human neutrophils drive skin autoinflammation by releasing interleukin (IL)-26.The Journal of experimental medicine · 2024Article
- Increased interleukin-26 in the peripheral joints of patients with axial spondyloarthritis and psoriatic arthritis, co-localizing with CD68-positive synoviocytes.Frontiers in immunology · 2024Article
- Plasma Levels of mir-34a-5p Correlate with Systemic Inflammation and Low Naïve CD4 T Cells in Common Variable Immunodeficiency.Journal of clinical immunology · 2023Article
- Identification of novel NFKB1 and ICOS frameshift variants in patients with CVID.Clinical and experimental immunology · 2023Article
- Genetics and clinical phenotypes in common variable immunodeficiency.Frontiers in genetics · 2023Article
- Seeking Relevant Biomarkers in Common Variable Immunodeficiency.Frontiers in immunology · 2022Review
- Convergence of cytokine dysregulation and antibody deficiency in common variable immunodeficiency with inflammatory complications.The Journal of allergy and clinical immunology · 2022Article
- Leveraging Systems Immunology to Optimize Diagnosis and Treatment of Inborn Errors of Immunity.Frontiers in systems biology · 2022Article
- Circulating bioactive bacterial DNA is associated with immune activation and complications in common variable immunodeficiency.JCI insight · 2021Article
- State-of-the-art diagnostic evaluation of common variable immunodeficiency.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2021Review
- Beyond monogenetic rare variants: tackling the low rate of genetic diagnoses in predominantly antibody deficiency.Cellular & molecular immunology · 2021Review
- Targeted Proteomics Reveals Inflammatory Pathways that Classify Immune Dysregulation in Common Variable Immunodeficiency.Journal of clinical immunology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCommon variable immunodeficiency (CVID) is an antibody deficiency treated with immunoglobulin; however, patients can have noninfectious inflammatory conditions that lead to heightened morbidity and mortality.
objectivesModular analyses of RNA transcripts in whole blood previously identified an upregulation of many interferon-responsive genes. In this study we sought the cell populations leading to this signature.
methodsLymphoid cells were measured in peripheral blood of 55 patients with CVID (31 with and 24 without inflammatory/autoimmune complications) by using mass cytometry and flow cytometry. Surface markers, cytokines, and transcriptional characteristics of sorted innate lymphoid cells (ILCs) were defined by using quantitative PCR. Gastrointestinal and lung biopsy specimens of subjects with inflammatory disease were stained to seek ILCs in tissues.
resultsThe linage-negative, CD127(+), CD161(+) lymphoid population containing T-box transcription factor, retinoic acid-related orphan receptor (ROR) γt, IFN-γ, IL-17A, and IL-22, all hallmarks of type 3 innate lymphoid cells, were expanded in the blood of patients with CVID with inflammatory conditions (mean, 3.7% of PBMCs). ILCs contained detectable amounts of the transcription factors inhibitor of DNA binding 2, T-box transcription factor, and RORγt and increased mRNA transcripts for IL-23 receptor (IL-23R) and IL-26, demonstrating inflammatory potential. In gastrointestinal and lung biopsy tissues of patients with CVID, numerous IFN-γ(+)RORγt(+)CD3(-) cells were identified, suggesting a role in these mucosal inflammatory states.
conclusionsAn expansion of this highly inflammatory ILC population is a characteristic of patients with CVID with inflammatory disease; ILCs and the interferon signature are markers for the uncontrolled inflammatory state in these patients.
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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.