Author

R. Woodson

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Immunology· 3 Microbiology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 4 Research Focus:host-pathogen & immune response· 4 Organism:mouse· 4 Research Focus:cell signaling & trafficking· 3 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Research Focus:development & morphogenesis· 1

Frequent Co-Authors

A. Smirnov· 4 shared C. L. Stallings· 4 shared D. Kreamalmeyer· 4 shared R. L. Kinsella· 4 shared N. Dubey· 3 shared S. K. Naik· 3 shared S. R. McKee· 3 shared S. M. Chavez· 2 shared

Activity by Year

2022-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 44 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

4 shared papersImmunology

A. Smirnov

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

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

S. K. Naik, M. E. McNehlan, Y. Mreyoud, R. L. Kinsella, A. Smirnov, C. S. Chowdhury, S. R. McKee, N. Dubey, R. Woodson, D. Kreamalmeyer, C. L. Stallings

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

bioRxiv · Oct 3, 2023 · PreprintImmunology

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

N. Dubey, R. Woodson, S. V. Hendrix, A. L. Rosen, R. L. Kinsella, S. R. McKee, M. Starick, N. Rivera-Espinal, S. K. Naik, A. Smirnov, D. Kreamalmeyer, A. L. Kau, C. L. Stallings

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.

bioRxiv · Mar 16, 2023Immunology

Autophagy protects against high-dose Mycobacterium tuberculosis infection

S. Feng, E. M. Nehls, R. L. Kinsella, S. M. Chavez, S. K. Naik, S. R. McKee, N. Dubey, A. Samuels, A. Swain, X. Cui, S. V. Hendrix, R. Woodson, D. Kreamalmeyer, A. Smirnov, M. N. Artyomov, , C. L. Stallings

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.

bioRxiv · Nov 4, 2022Microbiology

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

R. L. Kinsella, J. M. Kimmey, A. Smirnov, R. Woodson, M. R. Gaggioli, S. M. Chavez, D. Kreamalmeyer, C. L. Stallings

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

bioRxiv · Nov 4, 2022 · PreprintImmunology