Author

J. Amrute

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

Frequent Co-Authors

K. Lavine· 3 shared A. Bredemeyer· 2 shared C.-Y. Lin· 2 shared J. Jimenez· 2 shared P. Ma· 2 shared A. Koenig· 1 shared A. Parks· 1 shared A. Villanueva· 1 shared

Activity by Year

2021-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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3 shared papersImmunology

K. Lavine

Mutual co-authors in cluster

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3 papers

Recent·Most cited

CD40 is an immune checkpoint regulator that potentiates myocardial inflammation through activation and expansion of CCR2+ macrophages and CD8 T-cells

J. Jimenez, J. Amrute, P. Ma, X. Wang, R. Dai, K. Lavine

This study shows CD40 agonists promote myocardial inflammation by activating CCR2+ macrophages and CD8 T-cells, leading to heart failure.

bioRxiv · Mar 14, 2024 · PreprintImmunology

Expansion of Disease Specific Cardiac Macrophages in Immune Checkpoint Inhibitor Myocarditis

P. Ma, J. Liu, J. Qin, L. Lai, G. S. Heo, H. Luehmann, D. Sultan, A. Bredemeyer, G. Bajpai, G. Feng, J. Jimenez, A. Parks, J. Amrute, A. Villanueva, Y. Liu, , K. Lavine

This study identifies an inflammatory macrophage population expanded in ICI myocarditis, driven by IFN-γ signaling and T-cell interactions, suggesting IFN-γ blockade as a potential therapeutic strategy.

bioRxiv · Apr 28, 2023 · PreprintImmunology

Donor Macrophages Modulate Rejection after Heart Transplantation

B. Kopecky, H. Dun, J. Amrute, C.-Y. Lin, A. Bredemeyer, Y. Terada, P. Bayguinov, A. Koenig, C. Frye, J. Fitzpatrick, D. Kreisel, K. Lavine

This study identifies donor CCR2+ macrophages as key drivers of heart transplant rejection and shows that inhibiting MYD88 signaling in these cells extends graft survival.

bioRxiv · Sep 17, 2021Immunology