Christopher M. Sassetti

The paper shows human memory CD4+ T cells recognize both Mtb-infected and bystander macrophages, with some TCRs specifically recognizing infected cells.

Complete genomes from 151 clinical M. tuberculosis isolates show gene conversion between paralogs creating diversity hotspots in PE/PPE/ESX genes and T cell antigens, including PPE18.

The paper identifies SSR INDELs in Mycobacterium tuberculosis that alter antibiotic susceptibility through phylogenomic analysis and experimental validation.

This study identifies the GID/CTLH complex as a regulator of metabolism and innate immunity in macrophages infected with Mycobacterium tuberculosis through ubiquitylation profiling and functional analysis.

This study identifies cross-species blood transcriptional correlates of BCG-mediated protection against tuberculosis using a systems modeling framework, linking innate and adaptive immune processes to vaccine efficacy in humans and non-human primates.

This study identifies protective antibodies against Mycobacterium tuberculosis and shows that their Fc-effector function and Fab domains collaborate to restrict infection through immune cell reorganization.

This study identifies in vivo chemical-genetic interactions in tuberculosis that reveal novel drug targets and mechanisms, showing differences from in vitro results and highlighting metabolic dependencies affecting drug efficacy.

This paper introduces PCL analysis to predict small molecule mechanisms of action in Mycobacterium tuberculosis using PROSPECT data, achieving high sensitivity and precision in MOA prediction.

This study shows that impaired macrophage fatty acid metabolism limits Mycobacterium tuberculosis growth through multiple anti-microbial mechanisms.

The paper identifies the GID/CTLH complex as a host determinant suppressing antimicrobial responses against intracellular bacterial infections through a CRISPR screen in Mtb-infected macrophages.

The paper updates the MiniMUGA genotyping array's bioinformatic pipeline to enhance genetic QC in laboratory mice by improving marker annotation, consensus genotypes, and report usability.

The paper uses cross-species modeling to identify the unfolded protein response as a key factor in the transcriptional response to Mycobacterium tuberculosis infection.

The paper uses transposon mutagenesis and QTL mapping to identify host-pathogen genetic interactions affecting Mtb fitness in immunodivergent mice.

This study identifies host-pathogen genetic interactions influencing tuberculosis susceptibility using a genetically diverse mouse panel and Mtb mutants.

The paper introduces MiniMUGA, a genotyping array for mouse genetic QC, showing it effectively discriminates strains, detects genetic constructs, and identifies sex chromosome abnormalities.

This paper introduces a statistical method using Zero-Inflated Negative Binomial regression to identify genes with significant variability in insertion counts across multiple conditions in TnSeq data.

ORBIT enables high-throughput chromosomal engineering in mycobacteria without requiring custom double-stranded DNA substrates by combining recombination systems and reusable payload plasmids.

This study identifies CNBP as a regulator of c-Rel dependent IL-12β gene transcription and Th1 immunity, showing its role in macrophage function and resistance to toxoplasmosis.