Michael J. Bale

The paper identifies H3 serine 28 phosphorylation as a mechanism driving chromatin derepression and immune cell fate transitions by disrupting repressive chromatin domains.

The paper identifies NRF2-driven myeloid progenitor dysregulation that sustains immunosuppressive macrophages in tumors, showing NRF2 inhibition reduces their survival and enhances antitumor immunity.

The paper compares HIV-1 proviral defects in children and adults on ART, finding more deletions and defects in children, especially in env and tat regions.

This study identifies shared and distinct mechanisms of macrophage programming by IL4 and glucocorticoids, revealing GRIP1's role in integrating their effects on transcription and function.

This study shows that SARS-CoV-2 infection primes alveolar macrophages for enhanced antiviral responses against influenza A virus through epigenetic changes in IFN-I pathways.

The paper compares the fraction and total number of HIV-infected cells with unspliced RNA in controllers and non-controllers, finding that viremic control is linked to fewer infected cells, not a lower fraction of infected cells with HIV usRNA.

This study shows that bladder BCG immunotherapy reprograms hematopoietic stem cells to enhance anti-tumor immunity in mice and humans.

The paper identifies large T-cell clones producing infectious HIV-1 virus as a source of non-suppressible viremia despite ART adherence and no drug resistance.

HIV-DRLink detects linked HIV-1 drug resistance mutations in next-generation sequencing data to predict treatment failure.