Shen‐Ying Zhang

Humans homozygous for rare or common hypomorphic IL23R variants are prone to tuberculosis

Homozygosity for hypomorphic IL23R variants (G149R, G300V, R381Q) partly impairs IL-23-dependent IFN-γ production in patient cells; with L372F (effect inferred), they are enriched in tuberculosis, not MSMD or CMC patients.

Elevated levels of intracellular RNA lariats suppress the antiviral response

The paper shows that accumulation of intracellular RNA lariats in DBR1-null cells reduces antiviral response by desensitizing dsRNA sensors.

A flow cytometry-based assay to quantify the binding of transmembrane ligands to their cognate receptors using fluorescent virus-like particles

This paper introduces a flow cytometry-based assay using fluorescent virus-like particles to quantify transmembrane ligand-receptor binding, showing it can study patient-derived variants and enable single-cell analysis of multiple interactions.

Genetic adaptation to pathogens and increased risk of inflammatory disorders in post-Neolithic Europe

This study uses ancient genomics to show that genetic adaptation to pathogens in post-Neolithic Europe increased inflammatory disease risk through antagonistic pleiotropy.

Genome-wide detection of human variants that disrupt intronic branchpoints

The paper introduces BPHunter, a computational tool to detect intronic variants disrupting branchpoints, identifies known and novel mutations, and validates them experimentally.

Heterogeneity of monocyte subsets and susceptibility to influenza virus contribute to inter-population variability of protective immunity

The paper investigates monocyte subset heterogeneity and its impact on influenza virus susceptibility across populations, revealing differences in transcriptional responses and infection resistance between African and European ancestry individuals.

Negative selection on human genes causing severe inborn errors depends on disease outcome and both the mode and mechanism of inheritance

The paper develops CoNeS to assess negative selection on genes causing severe inborn errors, finding that disease outcome and inheritance mode/mechanism influence selection strength.