The CD47-SIRPα signaling axis functions as an innate immune checkpoint that inhibits phagocytosis in phagocytes and has been implicated as a promising target for cancer immunotherapy. The potential of macrocyclic peptides that target this signaling axis as immunotherapeutic agents has remained unknown, however.

Keywords. CD47, SIRPα, immunotherapy, tumor microenvironment, pediatric cancer, innate immune system, checkpoint inhibitor, phagocytosis

Anti-CD47-terapi — Många tumörceller överuttrycker CD47 för att undkomma immunosurveilansen hos värdimmunsystemet. CD47 binder till sitt CD47 is an antiphagocytic ligand broadly expressed on normal and malignant tissues that delivers an inhibitory signal through the receptor signal regulatory protein alpha (SIRPα). Inhibitors of the CD47-SIRPα interaction improve antitumor antibody responses by enhancing antibody-dependent cellular phagocytosis (ADCP) in xenograft models. Tuesday, June 23, 2020 NIH investigators hope CD47 study leads to broad-spectrum infectious diseases immunotherapy Colorized scanning electron micrograph of a cell (purple) infected with SARS-COV-2 virus particles (yellow), isolated from a patient sample. Image captured at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland. Introduction: CD47 is an anti-phagocytic ('don't eat me') signal overexpressed in many malignant diseases. It acts as myeloid immune checkpoint and thus has prognostic and therapeutic implications.

Cd47 immunotherapy

immunotherapy. Indeed, CD47 was found to be highly expressed in various hematological malignancies and solid tumors relative to their normal counterparts, and such increased expression was correlated with poor prognosis in patients with these malignancies [5–8]. In contrast, blockade of Based on this observation, CD47 has become a prominent target in the field of cancer immunotherapy. Indeed, pre-clinical studies have shown therapeutic benefit of anti-CD47 antibodies in solid cancers and most notably B-cell malignancies.

CD47 is a critical self-protective “don’t eat me” signal on multiple human cancers against macrophage immunosurveillance. Using human and mouse TNBC preclinical models, we evaluated the efficacy of PrCR-based immunotherapy by blocking CD47.

CD47 is a ubiquitously expressed immunoregulatory protein best known for its so-called 'don't eat me' function that prevents phagocytic removal of healthy cells by the immune system. Many types of cancer present high levels of this don't eat me signal on their surface, thereby disrupting anti-cancer immune responses. The CD47/signal regulatory protein alpha (SIRPα) axis is a critical regulator of myeloid cell activation and serves a broader role as a myeloid-specific immune checkpoint. CD47 is highly expressed on many different types of cancer, and it transduces inhibitory signals through SIRPα on macrophages and other myeloid cells.

En grupp svarade mot anti-CD47 och en annan inte. Den andra .edu/newsroom/articles/year-2020/cancer-immunotherapy-gut-bacteria.html.

NIH investigators hope CD47 study leads to infectious diseases immunotherapy. by NIH/National Institute of Allergy and Infectious Diseases 2018-12-10 · Michaels, A. D. et al. CD47 blockade as an adjuvant immunotherapy for resectable pancreatic cancer. Clin. Cancer Res. 24, 1415–1425 (2018).

The protein CD47 is expressed in high levels on the surface of many cancer cells, where it acts as a "don't eat me" signal to the immune system's macrophages, commonly known as white blood cells. 2019-12-11 · Up-regulation of an innate immunosuppressive pathway, CD47, the ligand of the negative immune checkpoint regulator SIRPα (signal regulatory protein alpha), was observed in NSCLC tumors during anti-angiogenic therapy. Further studies revealed that CD47 upregulation in refractory lung tumor models was mediated by TNF-α/NF-κB1 signal pathway.
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CD47 is found to be overexpressed on tumor cells and act as a don't eat me' signal, which contributes to immune evasion. immunotherapy. Indeed, CD47 was found to be highly expressed in various hematological malignancies and solid tumors relative to their normal counterparts, and such increased expression was correlated with poor prognosis in patients with these malignancies [5–8]. In contrast, blockade of Based on this observation, CD47 has become a prominent target in the field of cancer immunotherapy.

ITGB2 expression could be a predictor for combined therapy with anti-CD47 with antigen-4 (CTLA-4) was the first immune checkpoint used for immunotherapy.
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Agonist Immunotherapy Targets and Combination Therapies, 15-16 Nov 2018, and has demonstrated superior activity compared to CD47/CD40 antibody

1A). The high-expression of 2020-06-24 · The researchers say that by blocking CD47-mediated signalling with antibodies in mice infected with lymphocytic choriomeningitis virus, they demonstrated they could enhance the speed of pathogen clearance in a form of immunotherapy. CD47, a tumor cell surface marker, plays as “don't eat me signal” through binding its recept or SIRPα on macrophages and the antibody against CD47, which blocks interactions of CD47 with SIRPα, has been shown to lead to tumor destruction1. Cancer immunotherapy is a promising therapeutic intervention. However, complete and durable responses are only seen in a fraction of patients who have cancer. Although cells of the myeloid lineage frequently infiltrate tumors and limit therapeutic success, currently approved immunotherapies primarily target tumor-infiltrating T and natural killer lymphocytes. The inhibitory receptor signal CD47-signal regulatory protein α signaling system and its application to cancer immunotherapy.

The protein CD47 is expressed in high levels on the surface of many cancer cells, where it acts as a "don't eat me" signal to the immune system 's macrophages, commonly known as white blood cells.

http ancer immune responses. Here, we treated carcinogen-induced or transplantable mouse models of cancer by a CD47 blocking antibody that was at least as efficient as chemotherapy and that could be favorably combined with the anthracycline mitoxantrone in the context of carcinogen-induced ortho- 2021-03-01 2021-03-17 2019-03-14 2018-08-28 Multiple myeloma (MM) remains to be incurable despite recent therapeutic advances. CD47, an immune checkpoint known as the “don’t eat me” signal, is highly expressed on the surface of various cancers, allowing cancer cells to send inhibitory signals to macrophages and impede phagocytosis and immune response.

CD47 is an antiphagocytic ligand broadly expressed on normal and malignant tissues that delivers an inhibitory signal through the receptor signal regulatory protein alpha (SIRPα). Inhibitors of the CD47–SIRPα interaction improve antitumor antibody responses by enhancing antibody-dependent cellular phagocytosis (ADCP) in xe- nograft models.