A5041927773- Inflammasome and immune disorders
- IL-33, ST2, and ILC Pathways
- Immune Cell Function and Interaction
- Autoimmune and Inflammatory Disorders Research
- Viral-associated cancers and disorders
- Pediatric health and respiratory diseases
- Immune cells in cancer
- Cystic Fibrosis Research Advances
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Acute Myeloid Leukemia Research
- Chronic Lymphocytic Leukemia Research
- Advancements in Transdermal Drug Delivery
- NF-κB Signaling Pathways
- Telomeres, Telomerase, and Senescence
- Hematopoietic Stem Cell Transplantation
- Antimicrobial Peptides and Activities
- Cancer Cells and Metastasis
- Eosinophilic Disorders and Syndromes
- Single-cell and spatial transcriptomics
- Immune responses and vaccinations
- Hydrogen's biological and therapeutic effects
- 3D Printing in Biomedical Research
- Neonatal Respiratory Health Research
- Dermatology and Skin Diseases
- interferon and immune responses
Unilever (India)
2021
NIHR Leeds Musculoskeletal Biomedical Research Unit
2016-2020
National Institute for Health Research
2016-2020
University of Leeds
2017-2019
St James's University Hospital
2016-2018
University of Lausanne
2018
Wellcome Trust
2016-2018
Cystic Fibrosis (CF) is a monogenic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, resulting defective CFTR-mediated chloride and bicarbonate transport, with dysregulation of epithelial sodium channels (ENaC). These changes alter fluid electrolyte homeostasis result an exaggerated proinflammatory response driven, part, infection. We tested hypothesis that NLRP3 inflammasome activation ENaC upregulation drives innate-immune responses this...
Objective To assess the prevalence of MYD 88 L265P mutation and variants within NLRP 3 evaluate status oligoclonal hematopoiesis in 30 patients with Schnitzler syndrome (SchS). Methods Thirty SchS were recruited from clinical centers. Six known acquired cryopyrin‐associated periodic syndromes ( aCAPS ) included as controls. Allele‐specific oligonucleotide–polymerase chain reaction was used for detection variant, next‐generation sequencing applied to analyze 28 genes associated...
TNFAIP3 encodes the NF-κB regulatory protein A20. High-penetrance heterozygous mutations in cause a haploinsufficiency of A20 (HA20), inadequate inhibition pathway, and an early onset autoinflammatory disorder. However, clinical phenotype patients with HA20 varies greatly diagnoses prior to establishing genetic cause, included both autoimmune conditions. Here, we present first patient HA20, who was previously diagnosed AOSD but later found have novel variant successfully treated anti-IL6...
Challenges to the musculoskeletal system negatively impact quality of life people suffering from them, leading pain, a decline in mobility, genetic alterations, and potential disorders. The bone marrow (BM) forms an integral part responsible for erythropoiesis optimal survival various immune stem cells within BM. However, due its dynamic complex three-dimensional (3D) structure, replicating BM physiologically traditional two-dimensional (2D) cell culture settings is often challenging, giving...
The Schnitzler Syndrome (SchS) is an acquired, autoinflammatory condition successfully treated with IL-1 inhibition. two main defining features of this late-onset are neutrophilic urticarial dermatoses (NUD) and the presence IgM monoclonal component. While former aspect has been extensively studied in disease setting, enigmatic paraproteinaemia its potential consequential effects within SchS, not previously thoroughly addressed. Previous studies analyzing clonal B cell repertoires have...
Abstract Cystic Fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene and results defective CFTR-mediated chloride transport, dysregulation of epithelial sodium channels (ENaC) exaggerated innate immune responses. We tested hypothesis that upregulation ENaC drives autoinflammation this complex monogenic disease. show monocytes from patients with CF exhibit a systemic proinflammatory cytokine signature, associated anti-inflammatory M2-type...