Author

B. L. Knolhoff

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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Cancer Biology· 2 Immunology· 1

Signature Assays, Organisms & Methods

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Organism:mouse· 3 Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Approach:deep learning· 1 Research Focus:development & morphogenesis· 1 Research Focus:differential expression· 1

Frequent Co-Authors

c. zuo· 3 shared J. M. Baer· 3 shared A. Alarcon de la Lastra· 2 shared D. G. DeNardo· 2 shared G. D. Hogg· 2 shared L. Ding· 2 shared N. C. Borcherding· 2 shared R. C. Fields· 2 shared

Activity by Year

2021-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 44 mutual co-author links

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3 shared papersCancer Biology

c. zuo

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Author profile →

3 papers

Recent·Most cited

Context-dependent triggering of STING-interferon signaling by CD11b agonists supports anti-tumor immunity in mouse models and human cancer patients

X. Liu, G. D. Hogg, c. zuo, J. M. Baer, V. E. Lander, L. Kang, N. C. Borcherding, B. L. Knolhoff, R. E. Osterhout, A. V. Galkin, J. M. Bruey, L. L. Carter, C. Mpoy, J. K. Schwarz, H. Park, , D. DeNardo

This study identifies how CD11b agonists trigger STING-interferon signaling in tumor-associated macrophages to enhance anti-tumor immunity in mouse models and human cancer patients.

bioRxiv · Mar 22, 2022 · PreprintCancer Biology

Pancreas resident macrophage-induced fibrosis has divergent roles in pancreas inflammatory injury and PDAC

J. M. Baer, C. Zuo, L.-I. Kang, A. Alarcon de la Lastra, N. C. Borcherding, B. L. Knolhoff, S. J. Bogner, Y. Zhu, M. A. Lewis, N. Zhang, K.-w. Kim, R. C. Fields, J. C. Mills, L. Ding, G. J. Randolph, D. G. DeNardo

This study shows that pancreas resident macrophages (TRMs) have distinct roles in pancreatitis and pancreatic cancer, promoting fibrosis in inflammation but driving cancer progression.

bioRxiv · Feb 9, 2022 · PreprintImmunology

Macrophage proliferation machinery leads to PDAC progression, but susceptibility to innate immunotherapy.

D. G. DeNardo, C. Zuo, J. M. Baer, B. L. Knolhoff, J. I. Belle, X. Liu, G. D. Hogg, C. Fu, N. L. Kingston, M. A. Brenden, A. Alarcon De La Lastra, P. B. Dodhiawala, C. Zhou, A. James, L. Ding, , J. D. Weber

This study shows that TAM proliferation in PDAC is driven by CSF1 from fibroblasts, leading to immunosuppression and tumor progression, but also increasing sensitivity to CD40 agonist therapy.

bioRxiv · Nov 8, 2021 · PreprintCancer Biology