Last update 01 Nov 2024

HBsAg x CD28

Last update 01 Nov 2024

Basic Info

Related Targets

HBsAgCD28

Drugs associated with HBsAg x CD28

SCG-211

Target

CD28 x HBsAg

Mechanism

CD28 inhibitors [+1]

Active Org.-

Originator Org.

SCG Cell Therapy Pte. Ltd.Startup

Active Indication-

Inactive Indication

Hepatitis B, Chronic

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with HBsAg x CD28

100 Translational Medicine associated with HBsAg x CD28

0 Patents (Medical) associated with HBsAg x CD28

Literatures (Medical) associated with HBsAg x CD28

01 Nov 2023·Annals of clinical and laboratory science

Exhaustion of CD8+ T Cells in HBV Infection: Searching for Serological Markers.

Article

Author: Liu, Xian ; Peng, Lishan ; Feng, Jinpeng

OBJECTIVEChronic infection of the hepatitis B virus (HBV) is associated with the dysfunction and exhaustion of CD8+ T cells, which are crucial in controlling HBV. While clinical parameters provide insight into the state of HBV infection, the relationship between HBV biochemical parameters and CD8+ T cell exhaustion remains poorly understood. This study aimed to evaluate the expression of activation, exhaustion, and function-related markers in CD8+ T cells of HBV carriers, and to determine the potential of HBV clinical parameters as biomarkers for CD8+ T cell exhaustion.METHODSWe enrolled 93 patients with HBV and measured the expression levels of CD160, T cell Ig and mucin-domain containing-3 (Tim-3), programmed cell death protein 1 (PD-1), cytotoxic T-lymphocyte antigen 4 (CTLA-4), CD28, CD137, granzyme B, and perforin in CD8+ T cells using flow cytometry. HBV clinical parameters including, HBsAg, HBsAb, HBeAg, HBeAb, HBcAb, HBV DNA load, ALT, AST, ABil, and ALB, were measured in the blood samples.RESULTSPatients were divided into two groups, HBV DNA+, and HBV DNA-, based on whether their HBV DNA load was below the test baseline; ALT, AST, and CD160+CD8+ T cell percentages were significantly higher in the HBV DNA+ group than in the HBV DNA- group (P=0.0323; P=0.0072; P=0.0458). However, the granzyme B-expressing CD8+ T cell percentage in the HBV DNA-group was higher than the HBV DNA+ group (P=0.0497). In the HBV DNA+ group, CD160, Tim-3, CD28, and perforin were significantly correlated with ALT, granzyme B was significantly correlated with AST; however, there was no correlation with HBV DNA load.CONCLUSIONIt is possible to infer the level of CD8+ T cell exhaustion in patients with an HBV DNA load >10² copies/mL based on clinical parameters (such as ALT, AST, and ABIL).

01 Aug 2020·Scandinavian Journal of ImmunologyQ4 · MEDICINE

Effects of intrauterine exposure to maternal‐derived HBeAg on T cell immunity in cord blood

Q4 · MEDICINE

Article

Author: Ma, Yanchen ; Li, Jinna ; Liao, Dandan ; Gao, Yunfei ; Huang, Meiting ; Tang, Bo ; Liu, Zhihua ; Yin, Xueru ; Li, Yongyin

AbstractImmature immune system and immune tolerance induced by exposure to HBeAg in utero and/or shortly after infection in newborns were reportedly the causes of chronic HBV infection. To investigate the effect of maternal‐derived HBeAg on neonatal T cell immunity, we analysed and compared T cell phenotypes and functions among neonates born to HBsAg+/HBeAg+ mothers (HBeAg+ neonates), HBsAg+/HBeAg− mothers (HBeAg− neonates) and healthy control mothers (HC neonates), using flow cytometry. The results showed that neonatal T cell phenotypes were similar regardless of HBeAg exposure. Upon anti‐CD3 and anti‐CD28 stimulation in HBeAg+ neonates, CD4+ T cell production of IFN‐γ (P < .05) was significantly enhanced, while CD8+ T cells secreted significantly more IL‐2 compared with those in HBeAg− and HC groups (P < .05). Moreover, similar levels of IFN‐γ and IL‐10 were observed in the culture supernatant after stimulation with rHBsAg, rHBcAg or rHBeAg among HBeAg+, HBeAg− and HC neonates, whereas HBeAg+ neonates produced more TNF‐α than HBeAg− neonates upon stimulation with rHBcAg. In conclusion, the results indicated that the HBsAg+/HBeAg+ maternal environment did not influence the phenotypes of cord blood T cells but boosted neonatal non‐specific Th1‐type cytokine production.

01 Aug 2014·Experimental and clinical transplantation : official journal of the Middle East Society for Organ TransplantationQ4 · MEDICINE

Relation between costimulatory molecule polymorphism and hepatitis B infections in hematopoietic stem cell transplant recipients.

Q4 · MEDICINE

Article

Author: Karimi, Mohammad Hossein ; Saadi, Mahdiyar Iravani ; Geramizadeh, Bita ; Ramzi, Mani ; Yaghobi, Ramin ; Zakerinia, Maryam

OBJECTIVESCostimulatory gene polymorphisms have been proposed to affect the hepatitis B virus pathogenesis by affecting regulation of immune responses. The association between costimulatory molecule gene polymorphisms including CTLA4, PD.1, ICOS, and CD28 with hepatitis B virus infection has been evaluated in hematopoietic stem cell transplant patients.MATERIALS AND METHODSIn a cross-sectional study, single-nucleotide polymorphisms in the loci of the costimulatory molecules were analyzed in 3 study groups. Hepatitis B virus infection was evaluated in plasma samples of each allogeneic and autologous hematopoietic stem cell transplant patients by a third generation HBsAg enzyme-linked immunosorbent assay kit according to the manufacturer 's instructions.RESULTSHepatitis B virus infection was found in 19 of 72 allogeneic (26.3%) and 26 of 59 autologous patients (44.1%). The T allele of CTLA4-318 and CC genotype of CD28+17 polymorphisms are significantly more frequent in hepatitis B virus-infected allogeneic hematopoietic stem cell transplant patients. The CC genotype of CD28 +17 was seen more frequently in hepatitis B virus-infected allogeneic hematopoietic transplant patients. The C allele of the PD.1.9 was seen more frequently in hepatitis B virus-infected allogeneic hematopoietic patients experiencing graft-versus-host disease. Also, the frequency of CT genotype and T allele of the PD.1.9 was significantly increased in hepatitis B virus-infected allogeneic hematopoietic stem cell transplant patients experiencing low-grade graft-versus-host disease.CONCLUSIONSAssociations of CTLA4 -318 and CD28 +17 with hepatitis B virus infection in allogeneic hematopoietic stem cell transplant patients was reported, also it was determined that PD.1.9 genotypes and hepatitis B virus infection in allogeneic hematopoietic stem cell transplant patients experiencing low-grade graft-versus-host disease was associated. However, better evaluations of the relations between costimulatory gene polymorphisms with hepatitis B virus infection in hematopoietic stem cell transplant patients requires further investigations.

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