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Last update 23 Jan 2025

CD39 x CD8A

Last update 23 Jan 2025

Basic Info

Related Targets

CD39CD8A

Drugs associated with CD39 x CD8A

Target ENTPD1/CD8A Bispecific antibody(Mozart Therapeutics)

Target

CD39 x CD8A

Mechanism

CD39 inhibitors [+1]

Active Org.

Mozart Therapeutics, Inc.Startup

Originator Org.

Mozart Therapeutics, Inc.Startup

Active Indication

Autoimmune Diseases

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CD39 x CD8A

100 Translational Medicine associated with CD39 x CD8A

0 Patents (Medical) associated with CD39 x CD8A

Literatures (Medical) associated with CD39 x CD8A

01 Nov 2024·Kidney International

Evaluation of non-invasive biomarkers of kidney allograft rejection in a prospective multicenter unselected cohort study (EU-TRAIN)

Article

Author: Randoux-Lebrun, Christine ; Dragun, Duska ; Moreso, Francesc ; Demotes, Jacques ; Raynaud, Marc ; Berney, Thierry ; Legendre, Christophe ; Halleck, Fabian ; Racapé, Maud ; Villard, Jean ; Heidecke, Harald ; Le Mai, Hoa ; Aubert, Olivier ; Catar, Rusan Ali ; Gourraud, Pierre-Antoine ; Crespo, Elena ; Nguyen, Thi-Van-Ha ; Bestard, Oriol ; Papuchon, Emmanuelle ; Budde, Klemens ; Elias, Michelle ; Papalois, Vassilios ; Potena, Luciano ; Goutaudier, Valentin ; Girardin, François ; Loupy, Alexandre ; Philippe, Aurélie ; Yaiche, Sarhan ; Vicaut, Éric ; Brouard, Sophie ; Danger, Richard ; Taupin, Jean-Luc ; Bouton, Didier ; Lefaucheur, Carmen ; Zaidan, Mohamad ; Giral, Magali

Non-invasive biomarkers are promising tools for improving kidney allograft rejection monitoring, but their clinical adoption requires more evidence in specifically designed studies. To address this unmet need, we designed the EU-TRAIN study, a large prospective multicentric unselected cohort funded by the European Commission. Here, we included consecutive adult patients who received a kidney allograft in nine European transplant centers between November 2018 and June 2020. We prospectively assessed gene expression levels of 19 blood messenger RNAs, four antibodies targeting non-human leukocyte antigen (HLA) endothelial antigens, together with circulating anti-HLA donor-specific antibodies (DSA). The primary outcome was allograft rejection (antibody-mediated, T cell-mediated, or mixed) in the first year post-transplantation. Overall, 412 patients were included, with 812 biopsies paired with a blood sample. CD4 gene expression was significantly associated with rejection, while circulating anti-HLA DSA had a significant association with allograft rejection and a strong association with antibody-mediated rejection. All other tested biomarkers, including AKR1C3, CD3E, CD40, CD8A, CD9, CTLA4, ENTPD1, FOXP3, GZMB, ID3, IL7R, MS4A1, MZB1, POU2AF1, POU2F1, TCL1A, TLR4, and TRIB1, as well as antibodies against angiotensin II type 1 receptor, endothelin 1 type A receptor, C3a and C5a receptors, did not show significant associations with allograft rejection. The blood messenger RNAs and non-HLA antibodies did not show an additional value beyond standard of care monitoring parameters and circulating anti-HLA DSA to predict allograft rejection in the first year post-transplantation. Thus, our results open avenues for specifically designed studies to demonstrate the clinical relevance and implementation of other candidate non-invasive biomarkers in kidney transplantation practice.

Frontiers in Immunology

Immune cell expression patterns of CD39/CD73 ectonucleotidases in rodent models of cardiac arrest and resuscitation

Article

Author: Shinozaki, Koichiro ; Nandurkar, Harshal ; Robson, Simon C ; Aoki, Tomoaki ; Nakamura, Eriko ; Murao, Atsushi ; Kim, Sun Jung ; Yin, Tai ; Endo, Yusuke ; Hayashida, Kei ; Diamond, Betty ; Wang, Ping ; Wong, Vanessa ; Becker, Lance B

BackgroundCardiac arrest (CA) is a significant public health concern. There is the high imminent mortality and survival in those who are resuscitated is substantively compromised by the post-CA syndrome (PCAS), characterized by multiorgan ischemia–reperfusion injury (IRI). The inflammatory response in PCAS is complex and involves various immune cell types, including lymphocytes and myeloid cells that have been shown to exacerbate organ IRI, such as myocardial infarction. Purinergic signaling, as regulated by CD39 and CD73, has emerged as centrally important in the context of organ-specific IRI. Hence, comprehensive understanding of such purinergic responses may be likewise imperative for improving outcomes in PCAS.MethodsWe have investigated alterations of immune cell populations after CA by utilizing rodent models of PCAS. Blood and spleen were collected after CA and resuscitation and underwent flow cytometry analysis to evaluate shifts in CD3+CD4+ helper T cells, CD3+CD8a+ cytotoxic T cells, and CD4/CD8a ratios. We then examined the expression of CD39 and CD73 across diverse cell types, including myeloid cells, T lymphocytes, and B lymphocytes.ResultsIn both rat and mouse models, there were significant increases in the frequency of CD3+CD4+ T lymphocytes in PCAS (rat, P < 0.01; mouse, P < 0.001), with consequently elevated CD4/CD8a ratios in whole blood (both, P < 0.001). Moreover, CD39 and CD73 expression on blood leukocytes were markedly increased (rat, P < 0.05; mouse, P < 0.01 at 24h). Further analysis in the experimental mouse model revealed that CD11b+ myeloid cells, with significant increase in their population (P < 0.01), had high level of CD39 (88.80 ± 2.05 %) and increased expression of CD73 (P < 0.05). CD19+ B lymphocytes showed slight increases of CD39 (P < 0.05 at 2h) and CD73 (P < 0.05 at 2h), while, CD3+ T lymphocytes had decreased levels of them. These findings suggested a distinct patterns of expression of CD39 and CD73 in these specific immune cell populations after CA.ConclusionsThese data have provided comprehensive insights into the immune response after CA, highlighting high-level expressions of CD39 and CD73 in myeloid cells.

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