KADAR HUMAN LEUKOCYTE ANTIGEN-G (HLAG) DAN TUMOR NERCROSIS FAKTOR ALPHA (TNF-a) PADA ABORTUS DAN KEHAMILAN NORMAL

2016 ◽  
Vol 2 (2) ◽  
Author(s):  
Kresno Condro Adhi ◽  
Sri Sulistywati ◽  
Supriyadi Hari Respati
Keyword(s):  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Leukocyte Antigen ◽  
Human Leukocyte Antigen G

Expression of human leukocyte antigen-G in systemic lupus erythematosus

2008 ◽  
Vol 69 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Silvia Rosado ◽  
Gema Perez-Chacon ◽  
Susana Mellor-Pita ◽  
Inmaculada Sanchez-Vegazo ◽  
Carmen Bellas-Menendez ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Human Leukocyte Antigen ◽  
Lupus Erythematosus ◽  
Human Leukocyte ◽  
Systemic Lupus ◽  
Leukocyte Antigen ◽  
Human Leukocyte Antigen G

scholarly journals Human Herpesvirus 6A and 6B inhibit in vitro angiogenesis by induction of Human Leukocyte Antigen G

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Roberta Rizzo ◽  
Maria D’Accolti ◽  
Daria Bortolotti ◽  
Francesca Caccuri ◽  
Arnaldo Caruso ◽  
...  
Keyword(s):  
Human Leukocyte Antigen ◽  
Human Herpesvirus ◽  
Human Leukocyte ◽  
Leukocyte Antigen ◽  
Human Leukocyte Antigen G ◽  
In Vitro Angiogenesis

scholarly journals Targeting human leukocyte antigen G with chimeric antigen receptors of natural killer cells convert immunosuppression to ablate solid tumors

2021 ◽  
Vol 9 (10) ◽  
pp. e003050
Author(s):  
Chia-Ing Jan ◽  
Shi-Wei Huang ◽  
Peter Canoll ◽  
Jeffrey N Bruce ◽  
Yu-Chuan Lin ◽  
...  
Keyword(s):  
Human Leukocyte Antigen ◽  
Natural Killer ◽  
Solid Tumors ◽  
Low Dose ◽  
Human Leukocyte ◽  
Leukocyte Antigen ◽  
Low Dose Chemotherapy ◽  
Human Leukocyte Antigen G

BackgroundImmunotherapy against solid tumors has long been hampered by the development of immunosuppressive tumor microenvironment, and the lack of a specific tumor-associated antigen that could be targeted in different kinds of solid tumors. Human leukocyte antigen G (HLA-G) is an immune checkpoint protein (ICP) that is neoexpressed in most tumor cells as a way to evade immune attack and has been recently demonstrated as a useful target for chimeric antigen receptor (CAR)-T therapy of leukemia by in vitro studies. Here, we design and test for targeting HLA-G in solid tumors using a CAR strategy.MethodsWe developed a novel CAR strategy using natural killer (NK) cell as effector cells, featuring enhanced cytolytic effect via DAP12-based intracellular signal amplification. A single-chain variable fragment (scFv) against HLA-G is designed as the targeting moiety, and the construct is tested both in vitro and in vivo on four different solid tumor models. We also evaluated the synergy of this anti-HLA-G CAR-NK strategy with low-dose chemotherapy as combination therapy.ResultsHLA-G CAR-transduced NK cells present effective cytolysis of breast, brain, pancreatic, and ovarian cancer cells in vitro, as well as reduced xenograft tumor growth with extended median survival in orthotopic mouse models. In tumor coculture assays, the anti-HLA-G scFv moiety promotes Syk/Zap70 activation of NK cells, suggesting reversal of the HLA-G-mediated immunosuppression and hence restoration of native NK cytolytic functions. Tumor expression of HLA-G can be further induced using low-dose chemotherapy, which when combined with anti-HLA-G CAR-NK results in extensive tumor ablation both in vitro and in vivo. This upregulation of tumor HLA-G involves inhibition of DNMT1 and demethylation of transporter associated with antigen processing 1 promoter.ConclusionsOur novel CAR-NK strategy exploits the dual nature of HLA-G as both a tumor-associated neoantigen and an ICP to counteract tumor spread. Further ablation of tumors can be boosted when combined with administration of chemotherapeutic agents in clinical use. The readiness of this novel strategy envisions a wide applicability in treating solid tumors.

Post-transplant increase in soluble human leukocyte antigen-G associated with non-severe cardiac allograft vasculopathy

2013 ◽  
Vol 74 (3) ◽  
pp. 318-324 ◽  
Author(s):  
R.M. Blanco-García ◽  
M.R. López-Álvarez ◽  
I.P. Garrido ◽  
G. Salgado-Cecilia ◽  
J.A. Campillo ◽  
...  
Keyword(s):  
Human Leukocyte Antigen ◽  
Human Leukocyte ◽  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Allograft Vasculopathy ◽  
Leukocyte Antigen ◽  
Post Transplant ◽  
Human Leukocyte Antigen G

Correlation of Human Leukocyte Antigen-G (HLA-G) Expression and Disease Progression in Epithelial Ovarian Cancer

2009 ◽  
Vol 16 (11) ◽  
pp. 1103-1111 ◽  
Author(s):  
Yong Wook Jung ◽  
Young Tae Kim ◽  
Sang Wun Kim ◽  
Sunghoon Kim ◽  
Jae Hoon Kim ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Human Leukocyte Antigen ◽  
Epithelial Ovarian Cancer ◽  
Disease Progression ◽  
Human Leukocyte ◽  
Leukocyte Antigen ◽  
Human Leukocyte Antigen G

scholarly journals A Unique Regulation Region in the 3′ UTR of HLA-G with a Promising Potential

2020 ◽  
Vol 21 (3) ◽  
pp. 900 ◽  
Author(s):  
Adi Reches ◽  
Orit Berhani ◽  
Ofer Mandelboim
Keyword(s):  
Human Leukocyte Antigen ◽  
Expression Pattern ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Human Leukocyte ◽  
Hla Class I ◽  
Leukocyte Antigen ◽  
Distinct Site ◽  
Human Leukocyte Antigen G ◽  
Classical Human Leukocyte Antigen

Human leukocyte antigen G (HLA-G) is a non-classical human leukocyte antigen (HLA) class I protein that interacts with inhibitory receptors and is commonly overexpressed in various cancers, thereby establishing itself as an inhibitory checkpoint immune ligand. It is also expressed in trophoblast cells during pregnancy and protects the fetus from immune rejection. Despite its crucial role and its intriguing expression pattern, the regulation of HLA-G’s expression is only partially understood. HLA-G’s mRNA is expressed in many tissues but the protein expression is restricted only to the cells mentioned above. Therefore, we suggest that HLA-G is post-transcriptionally regulated. Here, we reveal a distinctive site present only in the 3′ Untranslated region (UTR) of HLA-G, which might explain its unique expression pattern. Consequently, we attempted to find binding factors such as RNA binding proteins (RBPs) and microRNAS (miRs) that regulate HLA-G expression by interacting with this distinct site present in its 3′ UTR. Our research indicates that this site should be further studied in order to reveal its significance.

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