Eugene M. Oltz

A CRISPRi screen identifies SON and MAP4K1 as regulators of IL-22 and IL-17 expression in innate lymphoid cells, revealing new therapeutic targets for immune-mediated diseases.

This study develops an in vitro model of terminal CD8 T cell dysfunction and epigenetic stabilization, revealing stable exhaustion signatures and impaired functionality.

This study uses an automated behavioral system and transcriptomic analysis to identify cognitive impairments in mice with long COVID, finding similar transcriptomic changes to humans.

The paper identifies two enhancers regulating IL-22 expression in type 3 lymphoid cells, showing distinct roles in different subsets and functions in disease models.

This study examines how glycosylation mutations in the NTD of the SARS-CoV-2 XEC variant affect neutralizing antibody responses, cell-cell fusion, and spike stability.

The paper shows that cohesin loading from Vβ promoters or enhancers initiates loop extrusion across the Tcrb locus, enabling long-range recombination.

This study evaluates neutralization, infectivity, and stability of JN.1-derived SARS-CoV-2 subvariants, finding that DelS31 mutation in the NTD reduces nAb titers, impairs infectivity, and increases spike stability.

This study evaluates neutralization resistance, infectivity, and membrane fusion of JN.1-derived SARS-CoV-2 subvariants SLip, FLiRT, and KP.2, identifying key mutations affecting antibody sensitivity and spike function.

This study compares immune evasion, antigenicity, and cell-cell fusion properties of SARS-CoV-2 BA.2.87.1 and JN.1 variants, finding BA.2.87.1 shows less neutralization escape and higher infectivity than JN.1 and XBB.1.5.

This study compares immune evasion, infectivity, and fusogenicity of SARS-CoV-2 variants BA.2.86 and FLip using neutralization assays and cell-based experiments.

The paper maps promoter interactions in human ILC3s using PCHi-C and links GWAS risk variants to target genes, identifying new autoimmune disease risk genes.

This study characterizes epigenetic aging in human classical monocytes, identifying age-associated DNA methylation changes and their links to gene expression and disease associations.