2023
DOI: 10.1016/j.intimp.2023.110557
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CD24 blockade as a novel strategy for cancer treatment

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Cited by 4 publications
(4 citation statements)
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“…Understanding the interplay between CD24 and NKG2D opens new avenues for cancer immunotherapy. Strategies that target CD24 expression or function in cancer cells could enhance NKG2D-mediated immune responses, potentially overcoming immune evasion mechanisms and improving the efficacy of treatments designed to activate NK and T cells against cancer (15,167). This highlights the importance of exploring the roles of CD24 and NKG2D in cancer immunity and the potential for therapeutic interventions that modulate their activity.…”
Section: Cd24 and Nkg2d Receptormentioning
confidence: 99%
See 1 more Smart Citation
“…Understanding the interplay between CD24 and NKG2D opens new avenues for cancer immunotherapy. Strategies that target CD24 expression or function in cancer cells could enhance NKG2D-mediated immune responses, potentially overcoming immune evasion mechanisms and improving the efficacy of treatments designed to activate NK and T cells against cancer (15,167). This highlights the importance of exploring the roles of CD24 and NKG2D in cancer immunity and the potential for therapeutic interventions that modulate their activity.…”
Section: Cd24 and Nkg2d Receptormentioning
confidence: 99%
“…One of these mechanisms involves the upregulation of specific anti-phagocytic membrane proteins often referred to as "don't eat me" signals. These proteins include cluster of differentiation 47 (CD47) (13), cluster of differentiation 24 (CD24) (14,15), PD-L1 ( 16), the beta-2 microglobulin (b2M) subunit of the major histocompatibility class I complex (MHC-I) (17), stanniocalcin 1 (STC-1) (18), and GD2 (19). Phagocytosis is typically assisted by inherent "eat me" signals that serve as ligands for phagocytic receptors.…”
Section: Introductionmentioning
confidence: 99%
“…Cancer stemness refers to the self-renewal and propagation abilities of cancer stem cells (CSCs), which play a critical role in tumor aggressiveness, drug resistance, and metastasis [89]. CSCs can be identified by several markers, including CD44, CD24, CD133, LGR5, SOX2, AQP5, ESA, PAF1, and CXCR4, although none of these markers is highly specific [90][91][92][93][94]. As a central component of the TME, CAFs are believed to interact with CSCs and maintain a favorable tumor niche, mainly through paracrine signaling [95].…”
Section: Cafs Contribute To Cancer Stemnessmentioning
confidence: 99%
“…Recent research has shown that CD24, which is overexpressed on tumor cells, interacts with the inhibitory receptor Siglec-10 on macrophages ( 6 ). This interaction promotes immune escape of tumor cells and creates a new immune checkpoint in the form of a “don’t eat me” signal ( 7 , 8 ). Therefore, CD24 has become a potential therapeutic target for cancer treatments, including antibody drugs, gene therapy, chimeric antigen receptor (CAR) T cell therapy, and more ( 9 , 10 ).…”
Section: Introductionmentioning
confidence: 99%