CD24: from A to Z

Fang, Xueliang; Zheng, Pan; Tang, Jie; Liu, Yang

doi:10.1038/cmi.2009.119

Cited by 229 publications

(239 citation statements)

References 99 publications

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“…5 By interacting with Siglec-G/10, an immunoreceptor tyrosine-based inhibition motif (ITIM)-containing negative regulator of inflammation, CD24 has been shown to serve as an essential brake for inflammation induced by damageassociated molecular patterns (DAMPs). 6,7 Bacterial and viral-derived sialidases, which were previously considered virulence factors only in the context of pathogen growth, can disrupt the CD24-Siglec-G/10-mediated negative regulation mechanism by de-sialylation, thereby exacerbating bacteriainduced sepsis.…”

Section: Introductionmentioning

confidence: 99%

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CD24 blunts oral squamous cancer development and dampens the functional expansion of myeloid-derived suppressor cells

et al. 2016

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CD24 expression has been implicated in the oncogenesis of multiple types of cancer and high tumor expression is considered a poor prognosis factor; however, the role of CD24 in oral cancer progression is unknown. Unlike other cancer types, we found that higher CD24 levels in human oral cancers are correlated to lower clinical stage and better overall survival. We then dissected the role of CD24 and mechanisms in oral cancer pathogenesis in mice using a genetic strategy and demonstrated that CD24 deficiency increased the oral cavity tumor burden in response to the carcinogen 4-nitroquioline 1-oxide (4-NQO). Immune profile analysis showed a significant expansion as well as increased suppressive function of myeloid-derived suppressor cells (MDSCs) in CD24 ¡/¡ mice, but no apparent impairment in T cells, B cells, or dendritic cells. Further, studies with an orthotopically transplanted syngeneic squamous carcinoma model in the tongue of CD24 ¡/¡ and CD24 C/¡ mice confirmed the protective roles of CD24 against cancer. Moreover, the difference in tumor growth between CD24 ¡/¡ and CD24 C/¡ mice was blunted by immunodepletion of MDSCs. We conclude that CD24 expression impedes MDSC expansion and function, and thus slows oral cancer oncogenesis. This study is the first to examine the role of CD24 in a de novo oral cancer model, and it highlights the need to consider the immune regulatory roles of CD24 in the development of CD24-targeted therapy for cancer.

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Section: Introductionmentioning

confidence: 99%

“…6 CD24 plays important roles in immune regulation by providing co-stimulatory signals to T cells and B cells. 5,8 For example, CD24 is critical for T cell homeostasis. 9 Of further immunological relevance, dysregulation of CD24 has been implicated in the development of autoimmune diseases.…”

Section: Introductionmentioning

confidence: 99%

CD24 blunts oral squamous cancer development and dampens the functional expansion of myeloid-derived suppressor cells

et al. 2016

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“…CD24 is a small heavily glycosylated cell-surface protein that is linked to the membrane by a GPI anchor and localized in a lipid raft (11). In hematopoietic cells, CD24 is expressed on B cells, T cells, eosinophils, dendritic cells, and, most prominently, neutrophils (12).…”

mentioning

confidence: 99%

CD24-Triggered Caspase-Dependent Apoptosis via Mitochondrial Membrane Depolarization and Reactive Oxygen Species Production of Human Neutrophils Is Impaired in Sepsis

Parlato

Souza-Fonseca-Guimarães

Philippart

et al. 2014

The Journal of Immunology

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Apoptosis is the most common pathway of neutrophil death under both physiological and inflammatory conditions. In this study, we describe an apoptotic pathway in human neutrophils that is triggered via the surface molecule CD24. In normal neutrophils, CD24 ligation induces death through depolarization of the mitochondrial membrane in a manner dependent on caspase-3 and caspase-9 and reactive oxygen species. Proinflammatory cytokines such as TNF-α, IFN-γ, and GM-CSF upregulated the expression of CD24 in vitro, favoring the emergence of a new CD16high/CD24high subset of cultured neutrophils. We observed that CD24 expression (at both mRNA and protein levels) was significantly downregulated in neutrophils from sepsis patients but not from patients with systemic inflammatory response syndrome. This downregulation was reproduced by incubation of neutrophils from healthy controls with corticosteroids or with plasma collected from sepsis patients, but not with IL-10 or TGF-β. Decreased CD24 expression observed on sepsis neutrophils was associated with lack of functionality of the molecule, because cross-ligation of CD24 failed to trigger apoptosis in neutrophils from sepsis patients. Our results suggest a novel aspect of CD24-mediated immunoregulation and represent, to our knowledge, the first report showing the role of CD24 in the delayed/defective cell death in sepsis.

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“…CD24, also known as heat stable Ag, is a glycophosphatidylinositol-anchored cell surface glycoprotein expressed, among others, in immature T cells, most B lymphocytes, and dendritic cells (18,23,24). Its expression is very low in mature T cells but can be induced transiently on TCR stimulation (25,26).…”

mentioning

confidence: 99%

NFAT5 Regulates T Lymphocyte Homeostasis and CD24-Dependent T Cell Expansion under Pathologic Hypernatremia

Berga-Bolaños

Drews-Elger

Aramburu

et al. 2010

The Journal of Immunology

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Immune cells rely on the transcription factor NFAT5 to adapt to hypertonic stress. The hypertonicity-dependent role of NFAT5 in T cells in vivo remains unclear because mouse models of NFAT5 deficiency have produced substantially different T cell phenotypes. In this study, we analyzed the T cell compartment in NFAT5-null and T cell-specific NFAT5 knockout mice. We found that NFAT5-null mice had constitutive, pronounced hypernatremia and suffered a severe immunodeficiency, with T cell lymphopenia, altered CD8 naive/memory homeostasis, and inability to reject allogeneic tumors. By contrast, T cell-specific NFAT5 knockout mice had normal plasma tonicity, rejected allogeneic tumors, and exhibited only a mild, low-penetrance memory bias in CD8 cells. Notably, when T cells from these mice were cultured ex vivo in hypernatremic media, they exhibited features found in NFAT5-null mice, with pronounced naive/memory imbalance and impaired homeostatic survival in response to IL-7, as well as a severe inhibition of their mitogen-induced proliferation. By analyzing surface receptors whose expression might be affected in NFAT5-deficient cells, we identified CD24 as a novel NFAT5 target induced by hypertonicity both in vitro and in vivo, and required to sustain T cell expansion under osmostress. NFAT5 bound to the Cd24 promoter in response to hypertonicity facilitated the local derepression of chromatin and enhanced the expression of CD24 mRNA and protein. Altogether, our results indicate that the systemic hypernatremia of NFAT5-null mice is a major contributor to their immunodeficiency, and highlight the role of NFAT5 and CD24 in the homeostasis of T cells under osmostress in vivo.

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CD24: from A to Z

Cited by 229 publications

References 99 publications

CD24 blunts oral squamous cancer development and dampens the functional expansion of myeloid-derived suppressor cells

CD24 blunts oral squamous cancer development and dampens the functional expansion of myeloid-derived suppressor cells

CD24-Triggered Caspase-Dependent Apoptosis via Mitochondrial Membrane Depolarization and Reactive Oxygen Species Production of Human Neutrophils Is Impaired in Sepsis

NFAT5 Regulates T Lymphocyte Homeostasis and CD24-Dependent T Cell Expansion under Pathologic Hypernatremia

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