Paul J. Utz

The paper identifies a novel cancer susceptibility mutation in hfBCC patients by analyzing skin mutagenesis and its association with BCC and prostate cancer.

The paper identifies CD38 as a marker for pathogenic T cells in T1D and shows that anti-CD38 mAb selectively depletes these cells to prevent diabetes without affecting Tregs.

SPP1hi macrophages in RA synovial fibrin deposits promote tissue hyperplasia.

The paper uses serum proteomics to identify molecular signatures that classify lupus nephritis, differentiate disease activity and chronicity, and predict treatment response.

The paper shows EBV infects and reprograms autoreactive B cells into antigen-presenting cells in MS, driving pathogenic T cell responses.

This study examines immune dysregulation in Long COVID patients, finding persistent elevated anti-envelope and nucleocapsid antibodies and increased autoantibodies over six months.

This study identifies cytokines that enhance influenza vaccine antibody responses in human organoids and mice, showing their potential as adjuvants to improve vaccine efficacy.

This study identifies conserved myeloid subsets and disease-associated gene expression changes in kidney injury across lupus mouse models and human patients with lupus nephritis.

The paper identifies distinct type 1 immune networks associated with varying severities of restrictive lung disease following COVID-19.

This study identifies granzyme K as a driver of a novel complement activation pathway independent of classical, lectin, or alternative pathways.

This study shows that STING V154M mutation in non-hematopoietic cells activates autoreactive lymphocytes, leading to autoantibodies and lung inflammation in mice, mirroring SAVI in humans.

The paper develops SCENT, a method to create cell-type-specific enhancer-gene maps from single-cell multimodal data, identifying causal variants and genes for diseases.

This study shows that Xist ribonucleoprotein complexes drive sex-biased autoimmunity in males, leading to autoimmune pathology and reprogramming of immune cells to resemble female patterns.

The paper maps cell-type-specific eQTLs for HLA genes across multiple tissues and identifies dynamic regulation of HLA-DQ genes in immune cells.

The paper shows adipocytes regulate fibroblast function through cortisol signaling, and their loss leads to fibroblast dysfunction in inflammatory diseases.

The paper develops a framework to impute histone modification abundances and infer directional associations between them using neural processes, identifying novel interactions and changes post-vaccination.

The paper deconstructs RA synovium using single-cell data to identify six cell type abundance phenotypes associated with distinct inflammatory states.

The paper integrates transcriptome and clinical data to identify overlooked disease relationships, such as between myositis and interstitial cystitis.