Publications by authors named "A H Kragten"
Article Synopsis
- SARS-CoV-2-specific CD8 T cells play a crucial role in protecting against viral variants and reducing disease severity, especially in patients lacking cross-reactive antibodies.
- mRNA vaccines elicit strong immune responses, but the effectiveness among patients with chronic immune-mediated inflammatory disorders (IMIDs), particularly those on TNF inhibitors (TNFi), is less understood.
- Analysis revealed that both TNFi-treated and untreated inflammatory bowel disease (IBD) patients generate strong spike-specific CD8 T cell responses after mRNA vaccination, comparable to healthy individuals, indicating that vaccination is beneficial regardless of treatment status.
XPA is a central scaffold protein that coordinates the assembly of repair complexes in the global genome (GG-NER) and transcription-coupled nucleotide excision repair (TC-NER) subpathways. Inactivating mutations in XPA cause xeroderma pigmentosum (XP), which is characterized by extreme UV sensitivity and a highly elevated skin cancer risk. Here, we describe two Dutch siblings in their late forties carrying a homozygous H244R substitution in the C-terminus of XPA.
View Article and Find Full Text PDFObjectives: High-magnitude CD8 T cell responses are associated with mild COVID-19 disease; however, the underlying characteristics that define CD8 T cell-mediated protection are not well understood. The antigenic breadth and the immunodominance hierarchies of epitope-specific CD8 T cells remain largely unexplored and are essential for the development of next-generation broad-protective vaccines. This study identified a broad spectrum of conserved SARS-CoV-2 CD8 T cell epitopes and defined their respective immunodominance and phenotypic profiles following SARS-CoV-2 infection.
View Article and Find Full Text PDFCells employ global genome nucleotide excision repair (GGR) to eliminate a broad spectrum of DNA lesions, including those induced by UV light. The lesion-recognition factor XPC initiates repair of helix-destabilizing DNA lesions, but binds poorly to lesions such as CPDs that do not destabilize DNA. How difficult-to-repair lesions are detected in chromatin is unknown.
View Article and Find Full Text PDFArticle Synopsis
- * The transcription-coupled repair (TCR) pathway removes these DNA lesions, but the mechanism for restoring transcription afterward is not well understood.
- * The study reveals that the CSB protein in TCR helps load the PAF1 complex onto RNAPII, which is crucial for recovering transcription following UV damage by facilitating RNAPII's release from pauses and enhancing its elongation process.