Results 11 to 20 of about 38,336 (234)

Review immune response of targeting CD39 in cancer

open access: yesBiomarker Research, 2023
The ATP-adenosine pathway has emerged as a promising target for cancer therapy, but challenges remain in achieving effective tumor control. Early research focused on blocking the adenosine generating enzyme CD73 and the adenosine receptors A2AR or A2BR ...
Yao Liu   +7 more
doaj   +3 more sources

Thrombo-Inflammation: A Focus on NTPDase1/CD39 [PDF]

open access: yesCells, 2021
There is increasing evidence for a link between inflammation and thrombosis. Following tissue injury, vascular endothelium becomes activated, losing its antithrombotic properties whereas inflammatory mediators build up a prothrombotic environment.
Morello, Silvana   +3 more
openaire   +5 more sources

Human soluble CD39 displays substrate inhibition in a substrate-specific manner

open access: yesScientific Reports, 2023
CD39 (ectonucleoside triphosphate diphosphohydrolase-1; ENTPD1) metabolizes extracellular ATP and ADP to AMP. AMP is subsequently metabolized by CD79 to adenosine. CD39 activity is therefore a key regulator of purinergic signalling in cancer, thrombosis,
Venkat M. K. Vadlamani   +4 more
doaj   +1 more source

Assessment of CD4+ cells subpopulations with the expressing CD39 and CD73 ectonucleotidases in children with psoriasis

open access: yesМедицинская иммунология, 2022
Purinergic signaling modulates systemic and local inflammatory responses in immune-mediated and autoimmune diseases, including psoriasis. Extracellular ATP is an important factor of purinergic regulation, and its levels are regulated by catalytic effects
D. G. Kuptsova   +5 more
doaj   +1 more source

Cancer CD39 drives metabolic adaption and mal-differentiation of CD4+ T cells in patients with non-small-cell lung cancer

open access: yesCell Death and Disease, 2023
While ectonucleotidase CD39 is a cancer therapeutic target in clinical trials, its direct effect on T-cell differentiation in human non-small-cell lung cancer (NSCLC) remains unclear.
Ying Wang   +8 more
doaj   +1 more source

Protein kinase inhibitor ceritinib blocks ectonucleotidase CD39 – a promising target for cancer immunotherapy

open access: yesJournal for ImmunoTherapy of Cancer, 2022
Background An important mechanism, by which cancer cells achieve immune escape, is the release of extracellular adenosine into their microenvironment. Adenosine activates adenosine A2A and A2B receptors on immune cells constituting one of the strongest ...
Julie Pelletier   +9 more
doaj   +1 more source

CD39+ conventional CD4+ T cells with exhaustion traits and cytotoxic potential infiltrate tumors and expand upon CTLA-4 blockade

open access: yesOncoImmunology, 2023
Conventional CD4+ T (Tconv) lymphocytes play important roles in tumor immunity; however, their contribution to tumor elimination remains poorly understood.
Sabrina N. Bossio   +17 more
doaj   +1 more source

Expression of TIM3/VISTA checkpoints and the CD68 macrophage-associated marker correlates with anti-PD1/PDL1 resistance: implications of immunogram heterogeneity. [PDF]

open access: yes, 2020
Although immunotherapies have achieved remarkable salutary effects among subgroups of advanced cancers, most patients do not respond. We comprehensively evaluated biomarkers associated with the "cancer-immunity cycle" in the pan-cancer setting in order ...
Dressman, Devin   +13 more
core   +1 more source

Increased frequency of TIGIT+CD73-CD8+ T cells with a TOX+ TCF-1low profile in patients with newly diagnosed and relapsed AML

open access: yesOncoImmunology, 2021
The inhibitory receptor TIGIT, as well as theectonucleotidases CD39 and CD73 constitute potential exhaustion markers for T cells. Detailed analysis of these markers can shed light into dysregulation of the T-cell response in acute myeloid leukemia (AML ...
F. Brauneck   +11 more
doaj   +1 more source

Expansion of CD25-Negative Forkhead Box P3-Positive T Cells during HIV and Mycobacterium tuberculosis Infection [PDF]

open access: yes, 2017
Tuberculosis (TB) and HIV alter the immune system, and coinfected (HIV-TB) individuals usually present deregulations of T-lymphocytic immune response.
Ameri, Diego   +9 more
core   +2 more sources

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