Christophe Bourges
A5062712933- RNA regulation and disease
- Neurological diseases and metabolism
- interferon and immune responses
- NF-κB Signaling Pathways
- Inflammatory Bowel Disease
- Hereditary Neurological Disorders
- COVID-19 Clinical Research Studies
- SARS-CoV-2 and COVID-19 Research
- Kruppel-like factors research
- Peroxisome Proliferator-Activated Receptors
- T-cell and B-cell Immunology
- Ferroptosis and cancer prognosis
- Systemic Sclerosis and Related Diseases
- Peripheral Neuropathies and Disorders
- Nuclear Receptors and Signaling
- Environmental Chemistry and Analysis
- Wnt/β-catenin signaling in development and cancer
- Endoplasmic Reticulum Stress and Disease
- Epigenetics and DNA Methylation
- Liver Diseases and Immunity
- Cancer-related gene regulation
- Diabetes and associated disorders
- Fecal contamination and water quality
- Adenosine and Purinergic Signaling
- Water Quality and Pollution Assessment
The Francis Crick Institute
2022-2024
Addenbrooke's Hospital
2020-2022
University of Cambridge
2019-2022
Inserm
2013-2016
Centre d’Immunologie de Marseille-Luminy
2013-2016
Aix-Marseille Université
2013-2016
Centre National de la Recherche Scientifique
2013-2014
Anti tumour necrosis factor (anti-TNF) drugs increase the risk of serious respiratory infection and impair protective immunity following pneumococcal influenza vaccination. Here we report SARS-CoV-2 vaccine-induced immune responses breakthrough infections in patients with inflammatory bowel disease, who are treated either anti-TNF antibody, infliximab, or vedolizumab targeting a gut-specific anti-integrin that does not systemic immunity. Geometric mean [SD] anti-S RBD antibody concentrations...
Abstract Increasing rates of autoimmune and inflammatory disease present a burgeoning threat to human health 1 . This is compounded by the limited efficacy available treatments high failure during drug development 2 , highlighting an urgent need better understand mechanisms. Here we show how functional genomics could address this challenge. By investigating intergenic haplotype on chr21q22—which has been independently linked bowel disease, ankylosing spondylitis, primary sclerosing...
Still's disease, the paradigm of autoinflammation-cum-autoimmunity, predisposes for a cytokine storm with excessive T lymphocyte activation upon viral infection. Loss function purine nucleoside enzyme FAMIN is sole known cause monogenic disease. Here we discovered that FAMIN-enabled metabolon in dendritic cells (DCs) restrains CD4+ and CD8+ cell priming. DCs absent activity prime enhanced antigen-specific cytotoxicity, IFNγ secretion, expansion, resulting influenza A virus-specific...
The membrane‐bound Vanin‐1 pantetheinase regulates tissue adaptation to stress. We investigated Vnn1 expression and its regulation in liver. is expressed by centrolobular hepatocytes. Using novel tools, we identify a soluble form of mouse human serum show the contribution cysteine catalytic activity. that liver contributes secretion PPARalpha limiting factor production. Functional PPRE sites are identified promoter. These results indicate might be reliable reporter activity
Anti-TNF drugs, such as infliximab, are associated with attenuated antibody responses after SARS-CoV-2 vaccination. We aimed to determine how the anti-TNF drug infliximab and anti-integrin vedolizumab affect vaccine-induced neutralising antibodies against highly transmissible omicron (B.1.1.529) BA.1, BA.4 BA.5 (hereafter BA.4/5) variants, which possess ability evade host immunity and, together emerging sublineages, now dominating variants causing current waves of infection.
Vanin-1 is an epithelial pantetheinase, which regulates intestinal inflammation in mouse. We investigated whether human VNN1 levels could be associated to the susceptibility inflammatory bowel diseases (IBD) and explored participation of PPARg these processes.We studied expression colon biopsies from IBD patients. polymorphisms regulatory regions gene examined their genetic association with disease. Functional relevance single-nucleotide (SNPs) was assayed, we tested nuclear complexes...
Article1 April 2020Open Access Transparent process Resolving mechanisms of immune-mediated disease in primary CD4 T cells Christophe Bourges Cambridge Institute Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, Campus, University Cambridge, UK Department Medicine, School Clinical Addenbrooke's Hospital, Search for more papers by this author Abigail F Groff Stem Cell Regenerative Biology, Harvard University, MA, USA Oliver S Burren Chiara Gerhardinger Kaia...
Objective In the management of patients with IBD, there is a need to identify prognostic markers and druggable biological pathways improve mucosal repair probe efficacy tumour necrosis factor alpha biologics. Vnn1 pantetheinase that degrades pantetheine pantothenate (vitamin B 5 , precursor coenzyme A (CoA) biosynthesis) cysteamine. overexpressed by inflamed colonocytes. We investigated its contribution tolerance intestinal mucosa colitis-induced injury. Design performed an RNA sequencing...
Abstract Systemic sclerosis (SSc) is an autoimmune disease characterized by fibrosis of the skin and visceral organs vascular alterations. SSc pathophysiology involves systemic inflammation oxidative stress. Because vanin-1 gene (vnn1) encodes enzyme with pantetheinase activity that converts vasculoprotective pantethine into profibrotic pantothenic acid pro-oxidant cystamine, we tested this pathway in SSc. Activation vanin-1/pantetheinase was investigated wild-type BALB/c mice hypochlorous...
Liver is a major regulator of lipid metabolism and adaptation to fasting, process involving PPARalpha activation. We recently showed that the Vnn1 gene target in liver release Vanin-1 pantetheinase serum biomarker Here we set up screen identify new regulators fasting using as marker Mutagenized mice were screened for low expression. Functional interactions with investigated by combining transcriptomic, biochemical metabolic approaches. characterized mutant mouse which hepatic expression...
Abstract Increasing global rates of autoimmune and inflammatory disease present a burgeoning threat to human health 1 . This is compounded by the limited efficacy available treatments high failure during drug development 2 – underscoring an urgent need better understand mechanisms. Here we show how genetics could address this challenge. By investigating intergenic haplotype on chr21q22, independently linked bowel (IBD), ankylosing spondylitis, primary sclerosing cholangitis Takayasu’s...
ABSTRACT Deriving mechanisms of immune-mediated disease from GWAS data remains a formidable challenge, with attempts to identify causal variants being frequently hampered by linkage disequilibrium. To determine whether could be identified via their functional effects, we adapted massively-parallel reporter assay for use in primary CD4 T-cells, key effectors many diseases. Using the results guide further study, provide generalisable framework resolving non-coding associations – illustrated...
Numerous genomic loci have been implicated in autoimmune disorders, but attempts to identify causal variants, and thereby disease mechanisms, hampered by strong linkage disequilibrium; leaving most unresolved the potential of GWAS largely unfulfilled. To overcome this, we developed a massively-parallel reporter assay for use primary CD4 T-cells, key effector many diseases, sought resolve variants via their functional effects. This provided testable hypotheses into which illustrate using...