Calreticulin exposure dictates the immunogenicity of cancer cell death

By M. Obeid, A. Tesnière, François Ghiringhelli, G. Fimia, L. Apetoh, J. Perfettini, M. Castedo, G. Mignot, T. Panaretakis, N. Casares and 7 more. Nature Medicine, 2007

3,061 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/cae4cc491136715ea0ad456d7a08824a2ba90f26

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Citations in the corpus

The CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors (2012, neutral): “However, caution must be used in applying antiCD47 therapy in the context of ongoing or recent cytotoxic or inflammatory therapy, as the translocation of calreticulin to the cell surface upon conditions of cell stress may render normal cells susceptible to phagocytosis by nearby macrophages (38, 39)”
Systemic effects of local radiotherapy (2009, positive): “The recent identification of two mediators of this process, calreticulin (CRT) and high-mobility group protein B1 (HMGB1), has shed light on the mechanism by which the irradiated tumor becomes a robust source of antigens for an in situ auto-vaccination [5,34].”
Damage-Associated Molecular Patterns in Inflammatory Diseases (2018, background): “Calreticulin functions as an important effector of ICD by inducing the DC-mediated phagocytosis of tumor cells, which reduces the tumor growth in colon carcinoma (86).”
Immunological aspects of cancer chemotherapy (2008, background): “This applies to drugs that kill cancer cells through mitochondrial, lysosomal or endoplasmic reticulum stress (ER stress), as well as protein tyrosine kinase inhibitors, proteasome inhibitors or DNA-damaging agents (such as alkylating agents or topoisomerase inhibition”
Immunogenic and tolerogenic cell death (2009, background): “In an effort to reconcile these different data, it has been proposed that there are subtypes of cell death, such as immunogenic and non-immunogenic apoptosis, and that subtle differences in the composition of the cell surface and/or in the products that are secreted by the dying cells (which could i”
The P2X7 Receptor in Infection and Inflammation (2017, positive): “Immunogenicity of anthracyclin-stimulated cell death depends on the release of intracellular molecules such as calreticulin, high mobility group box 1 (HMGB1) protein, and ATP (Obeid et al., 2007; Ghiringhelli et al., 2009).”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “CALR translocation occurs as an early ICDassociated event, i.e., it occurs before PS exposure [878], and is mediated (at least in the case of chemotherapy-driven ICD) by three sequential signal transduction modules: (1) an ER stress module, which involves the phosphorylation of eukaryotic translatio”
Combination strategies with PD-1/PD-L1 blockade: current advances and future directions (2022, background): “Besides, some cytotoxic chemotherapeutic drugs such as anthracycline and oxaliplatin could induce immunogenic cell death and stimulate antitumor immune response [33, 34].”
Immunogenic death of colon cancer cells treated with oxaliplatin (2010, methodology): “Surface CRT serves as an engulfment signal (Obeid et al., 2007a, b) and similarly targets apoptotic cells for interaction with DCs and subsequent cross-presentation of tumor antigens (Zeng et al., 2006).”