C. L. Stallings

Type I IFN signaling in the absence of IRGM1 promotes M. tuberculosis replication in immune cells by suppressing T cell responses

This study shows that IRGM1 deletion increases type I IFN signaling, which suppresses T cell responses and promotes M. tuberculosis replication in immune cells.

ATG5 suppresses type I IFN-dependent neutrophil swarming and NETosis

This study shows that ATG5 suppresses type I IFN-induced neutrophil swarming and NETosis during M. tuberculosis infection, contributing to disease susceptibility when ATG5 is absent.

Transcription regulation by CarD in mycobacteria is guided by basal promoter kinetics

This study shows CarD regulates transcription in Mtb by affecting RPo stability, with activation on unstable promoters and repression on stable ones, influenced by DNA supercoiling.

Autophagy functions in lung macrophages and dendritic cells to regulate allergen-dependent inflammatory responses

This study identifies autophagy's role in lung macrophages and dendritic cells in suppressing TH17 responses and neutrophil accumulation in allergic inflammation, with allergen-dependent effects on TH2 responses and cytokine secretion.

Inducing vulnerability to InhA inhibition restores isoniazid susceptibility in drug resistant Mycobacterium tuberculosis

This paper identifies a compound, C10, that re-sensitizes drug-resistant Mycobacterium tuberculosis to isoniazid by exploiting a metabolic vulnerability, without altering InhA activity or INH-NAD levels.

Type I IFN signaling mediates NET release to promote Mycobacterium tuberculosis replication and granuloma caseation

This study shows that type I IFN signaling drives NET release in neutrophils, promoting Mtb replication and granuloma caseation.

Discovery, Synthesis, and Optimization of 1,2,4-Triazolyl Pyridines Targeting Mycobacterium tuberculosis

This paper discovers and optimizes a new series of 1,2,4-triazolyl pyridines that inhibit Mycobacterium tuberculosis growth with nanomolar activity and favorable pharmacokinetics.

Autophagy protects against high-dose Mycobacterium tuberculosis infection

This study shows autophagy in myeloid cells protects against high-dose Mycobacterium tuberculosis infection by limiting myeloid-derived suppressor cells and promoting T cell responses, distinct from its role in low-dose infection.

Autophagy is required to prevent early pro-inflammatory responses and neutrophil recruitment during Mycobacterium tuberculosis infection without affecting pathogen replication in macrophages

This study shows that ATG5 in CD11c+ cells suppresses pro-inflammatory cytokines and neutrophil recruitment during M. tuberculosis infection without affecting pathogen replication.

DciA helicase operators exhibit diversity across bacterial phyla

This study identifies diversity in DciA helicase operators across bacterial phyla through computational evolutionary analysis of domain architectures and sequence motifs.