Author

C. S. Moore

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

Biology Disciplines

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Immunology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 3 Research Focus:cell type annotation· 3 Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:differential expression· 2 Research Focus:host-pathogen & immune response· 2 Research Focus:cell-cell communication· 1 Assay:scRNA-seq· 1

Frequent Co-Authors

A. Droit· 2 shared A. P. Yeola· 2 shared C. Joly-Beauparlant· 2 shared J. Baillargeon· 2 shared M. Rangachari· 2 shared P. M. I. A. Doss· 2 shared A. C. Anderson· 1 shared A. R. Hemnes· 1 shared

Activity by Year

2019-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 34 mutual co-author links

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2 shared papersImmunology

A. Droit

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Myelin-reactive B cells exacerbate the severity of CD4+ T cell-driven CNS autoimmunity in an IL-23-dependent manner.

M. R. Fazazi, P. M. I. A. Doss, R. Pereira, N. Fudge, A. Regmi, C. Joly-Beauparlant, I. Akbar, A. P. Yeola, B. Mailhot, J. Baillargeon, P. Grenier, N. Bertrand, S. Lacroix, A. Droit, C. S. Moore, , M. Rangachari

This study shows that MOG-specific B cells worsen CD4+ T cell-driven CNS autoimmunity by promoting Th17 and Tph cell accumulation via IL-23.

bioRxiv · Sep 6, 2023Immunology

Myeloid Cell-Derived IL1β Contributes to Pulmonary Vascular Remodeling in Heart Failure with Preserved Ejection Fraction

V. Agrawal, J. A. Kropski, J. J. Gokey, E. Kobeck, M. B. Murphy, K. T. Murray, N. L. Fortune, C. S. Moore, D. F. Meoli, K. Monahan, Y. R. Su, T. Blackwell, D. K. Gupta, M. H. Talati, E. J. Carrier, , A. R. Hemnes

This study identifies myeloid cell-derived IL1β as a key driver of pulmonary vascular remodeling in HFpEF using a murine model and multi-omics approaches.

bioRxiv · May 18, 2023 · PreprintCell Biology

Male sex chromosomal complement exacerbates the pathogenicity of Th17 cells in a chronic model of CNS autoimmunity.

P. M. I. A. Doss, J. Baillargeon, A. P. Yeola, J. B. Williams, M. Leclercq, C. Joly-Beauparlant, M. Alpaugh, A. C. Anderson, A. Droit, H. Lassmann, C. S. Moore, M. Rangachari

This study shows male sex chromosomal complement increases Th17 cell pathogenicity in CNS autoimmunity, independent of hormones, through downregulation of Jarid1c.

bioRxiv · Jun 13, 2019 · PreprintImmunology