Isabelle Meyts
A5040384200- Immunodeficiency and Autoimmune Disorders
- Blood disorders and treatments
- Immune Cell Function and Interaction
- Parvovirus B19 Infection Studies
- interferon and immune responses
- Cytomegalovirus and herpesvirus research
- Respiratory viral infections research
- SARS-CoV-2 and COVID-19 Research
- Adenosine and Purinergic Signaling
- Cystic Fibrosis Research Advances
- Diabetes and associated disorders
- Asthma and respiratory diseases
- Genomics and Rare Diseases
- T-cell and B-cell Immunology
- Hematopoietic Stem Cell Transplantation
- Immune Response and Inflammation
- COVID-19 Clinical Research Studies
- Pneumonia and Respiratory Infections
- Peptidase Inhibition and Analysis
- Pneumocystis jirovecii pneumonia detection and treatment
- Inflammasome and immune disorders
- Platelet Disorders and Treatments
- NF-κB Signaling Pathways
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Chronic Lymphocytic Leukemia Research
KU Leuven
2016-2025
Universitair Ziekenhuis Leuven
2003-2024
Immunité et Cancer
2024
Research Network (United States)
2024
Research Foundation - Flanders
2023
Hospital Sant Joan de Déu Barcelona
2022
Institut de Recerca Sant Joan de Déu
2022
Hôpital Necker-Enfants Malades
2022
Vall d'Hebron Hospital Universitari
2022
Université Libre de Bruxelles
2022
Abstract We report the updated classification of inborn errors immunity, compiled by International Union Immunological Societies Expert Committee. This documents key clinical and laboratory features 55 novel monogenic gene defects, 1 phenocopy due to autoantibodies, that have either been discovered since previous update (published January 2020) or were characterized earlier but confirmed expanded in subsequent studies. While variants additional genes associated with immune diseases reported...
There is uncertainty about the impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in individuals with rare inborn errors immunity (IEI), a population at risk developing disease 2019. This relevant not only for these patients but also general population, because studies IEIs can unveil key requirements host defense.
Type I interferons (IFNs) are essential mediators of antiviral responses. These cytokines have been implicated in the pathogenesis autoimmunity, most notably systemic lupus erythematosus (SLE), diabetes mellitus, and dermatomyositis, as well monogenic type interferonopathies. Despite a fundamental role health disease, direct quantification IFNs has challenging. Using single-molecule array (Simoa) digital ELISA technology, we recorded attomolar concentrations IFNα healthy donors, viral...
Heterozygosity for human signal transducer and activator of transcription 3 (STAT3) dominant-negative (DN) mutations underlies an autosomal dominant form hyper-immunoglobulin E syndrome (HIES). We describe patients with recessive HIES due to loss-of-function a previously uncharacterized gene, ZNF341 is factor that resides in the nucleus, where it binds specific DNA motif present various genes, including STAT3 promoter. The patients' cells have low basal levels mRNA protein. autoinduction...
Autosomal recessive IRF7 and IRF9 deficiencies impair type I III IFN immunity underlie severe influenza pneumonitis. We report three unrelated children with A virus (IAV) infection manifesting as acute respiratory distress syndrome (IAV-ARDS), heterozygous for rare TLR3 variants (P554S in two patients P680L the third) causing autosomal dominant (AD) deficiency. AD deficiency can herpes simplex virus-1 (HSV-1) encephalitis (HSE) by impairing cortical neuron-intrinsic to HSV-1. TLR3-mutated...
Vaccination against measles, mumps, and rubella (MMR) yellow fever (YF) with live attenuated viruses can rarely cause life-threatening disease. Severe illness by MMR vaccines be caused inborn errors of type I and/or III interferon (IFN) immunity (mutations in IFNAR2, STAT1, or STAT2). Adverse reactions to the YF vaccine have remained unexplained. We report two otherwise healthy patients, a 9-yr-old boy Iran severe measles disease at 1 yr 14-yr-old girl Brazil viscerotropic 12 yr. The Iranian...
Multisystem inflammatory syndrome in children (MIS-C) is a rare and severe condition that follows benign COVID-19. We report autosomal recessive deficiencies of OAS1 , OAS2 or RNASEL five unrelated with MIS-C. The cytosolic double-stranded RNA (dsRNA)–sensing generate 2′-5′-linked oligoadenylates (2-5A) activate the single-stranded RNA–degrading ribonuclease L (RNase L). Monocytic cell lines primary myeloid cells OAS1, OAS2, RNase produce excessive amounts cytokines upon dsRNA acute...
Recessive or dominant inborn errors of type I interferon (IFN) immunity can underlie critical COVID-19 pneumonia in unvaccinated adults. The risk children, which is much lower than adults, remains unexplained. In an international cohort 112 children (<16 yr old) hospitalized for pneumonia, we report 12 (10.7%) aged 1.5–13 with (7 children), severe (3), and moderate (2) 4 the 15 known clinically recessive biochemically complete IFN immunity: X-linked TLR7 deficiency children) autosomal...
Autoantibodies neutralizing type I interferons (IFNs) can underlie critical COVID-19 pneumonia and yellow fever vaccine disease. We report here on 13 patients harboring autoantibodies IFN-α2 alone (five patients) or with IFN-ω (eight from a cohort of 279 (4.7%) aged 6–73 yr influenza pneumonia. Nine four had antibodies high low concentrations, respectively, IFN-α2, six two IFN-ω. The patients’ increased A virus replication in both A549 cells reconstituted human airway epithelia. prevalence...
Patients with autoimmune polyendocrinopathy syndrome type 1 (APS-1) caused by autosomal recessive AIRE deficiency produce autoantibodies that neutralize I interferons (IFNs)1,2, conferring a predisposition to life-threatening COVID-19 pneumonia3. Here we report patients NIK or RELB deficiency, specific of autosomal-dominant NF-κB2 also have neutralizing against IFNs and are at higher risk getting pneumonia. In these found only in individuals who heterozygous for variants associated both...