Recombinant soluble CD226 protein directly inhibits cancer cell proliferation in vitro

Hou, Shengke; Zheng, Xiaodong; Wei, Haiming; Tian, Zhigang; Sun, Rui

doi:10.1016/j.intimp.2014.01.012

Cited by 14 publications

(8 citation statements)

References 22 publications

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“…Regarding the function of sCD226 in cancer, several studies reported that sCD226 may block the cytotoxicity of NK cells by blocking CD155 or CD112 [18], and that sCD226 could directly inhibit the proliferation of cancer cells in vitro [19]. In aGVHD, Kanaya et al explained that binding of sCD226 to CD155 may cancel the inhibitory signals by TIGIT in T cells [16].…”

Section: Discussionmentioning

confidence: 99%

“…A soluble form of CD226 (sCD226), which is shed from the membrane type of CD226 (mCD226) in human serum, has been identi ed. The utility of sCD226 as a biomarker has been reported in acute graft-versus-host disease (aGVHD) [16,17] and some types of cancers [18][19][20]. As for autoimmune diseases, a more recent study found that serum sCD226 levels were associated with disease activity in rheumatoid arthritis (RA) [21].…”

Section: Introductionmentioning

confidence: 99%

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Association of Elevated Serum Soluble Cd226 Levels With the Disease Activity and Flares of Systemic Lupus Erythematosus

Nakano

Ayano

Kushimoto

et al. 2021

Preprint

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Background: CD226 is an activating receptor expressed on the cell surface of natural killer cells and T cells. A soluble form of CD226 (sCD226) is known to be shed from the membrane type of CD226 (mCD226). Although CD226 polymorphism and mCD226 are known to be involved in systemic lupus erythematosus (SLE), the involvement of sCD226 in SLE is still unknown. Therefore, we aimed to reveal the association of sCD226 with SLE.Methods: We measured serum sCD226 levels using an enzyme-linked immunosorbent assay in 58 SLE patients and 33 healthy controls (HCs) and evaluated their associations with SLE Disease Activity Index 2000 (SLEDAI-2K), clinical manifestations, and laboratory data. We defined the maximum values of sCD226 in HCs as a cut-off level and compared the cumulative probability of flare for patients with high and low sCD226 levels. Results: Serum sCD226 levels showed no significant differences between SLE patients and HCs. However, sCD226 levels were significantly elevated in active SLE patients with a SLEDAI-2K score of ≥20 compared with HCs. In SLE patients, sCD226 levels were significantly correlated with SLEDAI-2K scores and anti-dsDNA antibody titers. Moreover, the cumulative probability of flare was markedly higher in patients with high sCD226 than in those with low sCD226. In patients with neuropsychiatric involvement, sCD226 levels were elevated and reflected neuropsychiatric disease activity. Conclusion: Serum sCD226 levels were associated with disease activity and flares of SLE. Thus, it may be a useful biomarker for SLE, and its monitoring allows for more precise SLE management.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Association of Elevated Serum Soluble Cd226 Levels With the Disease Activity and Flares of Systemic Lupus Erythematosus

Nakano

Ayano

Kushimoto

et al. 2021

Preprint

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“…CD34 + Hematopoietic Stem Cells (HSCs) co-express PVR (44) that could promote their lysis by CTLs if these cells express DNAM-1 instead of the coinhibitory receptor TIGIT. DNAM-1 may also have direct inhibitory effects in leukemia and cervical cancer cells through ligation of PVR and the alternative receptor PVRL2 (PVR-like 2, CD112), in addition to immune activation (45). PVRL2 is also able to bind the same couple of stimulatory and inhibitory ligands and binds, additionally, another inhibitory receptor, CD112R.…”

Section: Pvr (Poliovirus Receptor Cd155) Is a Nectinlike Ligand And mentioning

confidence: 99%

Immune ligands for cytotoxic T Lymphocytes CTLS in cancer stem cells CSCS

Voutsadakis¹

2018

Front Biosci

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The immune system has come to the forefront of cancer therapeutics in recent years with the success of immune blockade inhibitors in a variety of cancers whose list is increasing with a quick pace. Despite the efficacy of these drugs across a significant part of the cancer spectrum, responses are still seen only in a minority of patients, that implies that most patients are refractory or promptly develop resistance to these agents. Mechanisms of this resistance are important to decipher as this knowledge may lead to the introduction of additional therapies or manipulations to modulate resistance. The cancer stem cell theory stipulates that a minority of cancer cells in a given tumor are responsible for self-renewal and bulk tumor propagation. These cells, in most instances, are rare and less proliferative but give rise to highly proliferative progeny. In addition, they are, in general, resistant to therapies and endowed with metastatic potential through a process called EMT (Epithelial to Mesenchymal Transition). Cancer stem cells resistance to treatments may relate to inherent insensitivity to external apoptotic stimuli and, thus, may extend to immune therapies by inhibiting the actions of Cytotoxic T Lymphocytes (CTLs) in the tumor micro-environment. This paper examines available data on expression and regulation of immune co-modulatory (co-stimulatory and co-inhibitory) ligands on cancer stem cells in order to devise strategies to circumvent resistance.

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“…Similar to the results seen for membrane‐bound DNAM‐1 with respect to anti‐tumour responses, the interaction of soluble DNAM‐1 with CD155 and CD112 also resulted in the inhibition of tumour growth in a dose‐dependent manner. It is also possible that soluble DNAM‐1 might inhibit the metastatic potential of cancer cells, although further work is required to confirm this …”

Section: Dnam‐1 In the Control Of Cancermentioning

confidence: 99%

“…It is also possible that soluble DNAM-1 might inhibit the metastatic potential of cancer cells, although further work is required to confirm this. 11,64 In coordination with extrinsic cellular mechanisms that drive the anti-tumour response, intrinsic cellular mechanisms ultimately enforce the over-expression of DNAM-1Ls on targets so that they are recognized and attacked by NK cells. DNAM-1Ls are expressed on the surface of many tumour cells, such as lung carcinoma, primary human leukaemia, myeloma, melanoma, neuroblastoma, ovarian cancer, colorectal carcinoma and Ewing sarcoma cells.…”

Section: Dnam-1 In the Control Of Cancermentioning

confidence: 99%

Critical roles of co‐activation receptor DNAX accessory molecule‐1 in natural killer cell immunity

2015

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SummaryNatural killer (NK) cells, which can exert early and powerful anti-tumour and anti-viral responses, are important components of the innate immune system. DNAX accessory molecule-1 (DNAM-1) is an activating receptor molecule expressed on the surface of NK cells. Recent findings suggest that DNAM-1 is a critical regulator of NK cell biology. DNAM-1 is involved in NK cell education and differentiation, and also plays a pivotal role in the development of cancer, viral infections and immune-related diseases. However, tumours and viruses have developed multiple mechanisms to evade the immune system. They are able to impair DNAM-1 activity by targeting the DNAM-1 receptor-ligand system. We have reviewed the roles of DNAM-1, and its biological functions, with respect to NK cell biology and DNAM-1 chimeric antigen receptor-based immunotherapy.

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Recombinant soluble CD226 protein directly inhibits cancer cell proliferation in vitro

Cited by 14 publications

References 22 publications

Association of Elevated Serum Soluble Cd226 Levels With the Disease Activity and Flares of Systemic Lupus Erythematosus

Association of Elevated Serum Soluble Cd226 Levels With the Disease Activity and Flares of Systemic Lupus Erythematosus

Immune ligands for cytotoxic T Lymphocytes CTLS in cancer stem cells CSCS

Critical roles of co‐activation receptor DNAX accessory molecule‐1 in natural killer cell immunity

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