Henning Boekhoff
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Henning Boekhoff has a total of 54 co-authors. Here are the top co-authors by number of shared publications:
- Afonso Teixeira da Mota
Gulbenkian Institute for Molecular Medicine, Lisbon, Portugal
10 shared publications - Bruno Silva-Santos
Affiliations Gulbenkian Institute for Molecular Medicine, Lisbon, Portugal, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal
10 shared publications - Carolina Jardim
IBET, Instituto de Biologia Experimental e Tecnologica, Apartado 12, 2781-901 Oeiras, Portugal
10 shared publications - Catarina Brito
BET, Instituto de Biologia Experimental e Tecnológica, Oeiras, Portugal
10 shared publications - Catarina Monteiro Gomes
BET, Instituto de Biologia Experimental e Biológica
10 shared publications - Elvira Pequeno Leites
Gulbenkian Institute for Molecular Medicine, Lisbon, Portugal
10 shared publications
Latest Publications
- 9 July 2025
- Published by American Association for Cancer Research (AACR) in Cancer Immunology Research
- p. OF1-OF19
Sustained Macrophage Reprogramming Is Required for CD8+ T Cell–dependent Long-Term Tumor Eradication
Tumor-associated macrophages (TAM) exhibit a dual role in tumor progression and antitumor immunity. However, understanding the functional states and molecular mechanisms of antitumor TAMs remains a challenge. Herein, we show that intratumoral administration of a combination of agonists against TLR3 and CD40 [hereafter termed myeloid cell treatment (MCT)] reprogrammed TAMs in situ to adopt a protective antitumor phenotype in an orthotopic mouse breast cancer model, and that this led to tumor regression. Single-cell RNA sequencing of TAMs from different tumor stages and after MCT revealed a transient antitumor TAM phenotype, present at 12 hours after MCT and characterized by markers such as inducible nitric oxide synthase and CD38, which was replaced by TAMs coexpressing tumor-limiting and tumor-promoting features by 72 hours after MCT. Maintenance of antitumor TAMs required repeated MCT administration, and this promoted the activation of CD8+ T cells and long-term tumor eradication. Mechanistically, reactive oxygen species and TNF-α were pivotal in TAM-mediated tumor control. Our findings uncover the vulnerability of transient TAM reprogramming and show that it can be overcome by repeated MCT administrations to sustain efficient antitumor immune responses.
- 9 July 2025
- Published by American Association for Cancer Research (AACR) in Cancer Immunology Research
- p. OF1-OF19
Sustained Macrophage Reprogramming Is Required for CD8+ T Cell–dependent Long-Term Tumor Eradication
Tumor-associated macrophages (TAM) exhibit a dual role in tumor progression and antitumor immunity. However, understanding the functional states and molecular mechanisms of antitumor TAMs remains a challenge. Herein, we show that intratumoral administration of a combination of agonists against TLR3 and CD40 [hereafter termed myeloid cell treatment (MCT)] reprogrammed TAMs in situ to adopt a protective antitumor phenotype in an orthotopic mouse breast cancer model, and that this led to tumor regression. Single-cell RNA sequencing of TAMs from different tumor stages and after MCT revealed a transient antitumor TAM phenotype, present at 12 hours after MCT and characterized by markers such as inducible nitric oxide synthase and CD38, which was replaced by TAMs coexpressing tumor-limiting and tumor-promoting features by 72 hours after MCT. Maintenance of antitumor TAMs required repeated MCT administration, and this promoted the activation of CD8+ T cells and long-term tumor eradication. Mechanistically, reactive oxygen species and TNF-α were pivotal in TAM-mediated tumor control. Our findings uncover the vulnerability of transient TAM reprogramming and show that it can be overcome by repeated MCT administrations to sustain efficient antitumor immune responses.