AI Article Synopsis
- BTLA is an inhibitory immune checkpoint that interacts with HVEM to regulate immune balance and maintain immune tolerance on the same cell, while also affecting different immune cells to suppress immune responses.
- Dysregulation of the BTLA/HVEM interaction can lead to impaired immune cell function, allowing tumor cells to evade immune detection and progress.
- Research indicates that BTLA and HVEM are often abnormally expressed in various tumors, making them potential targets for future immunotherapy approaches in treating hematologic malignancies.
Article Abstract
B and T lymphocyte attenuator (BTLA) is an inhibitory immune checkpoint, which typically interacts with herpesvirus entry mediator (HVEM) and plays a crucial role in regulating immune balance. BTLA interacts with its ligand HVEM in a cis manner on the surface of the same immune cell to maintain immune tolerance, while trans interactions on the surface of different immune cells mediate immunosuppressive effects. Dysregulation of the BTLA/HVEM axis can impair the functions of immune cells, particularly T lymphocytes, promoting immune escape of tumor cells and ultimately leading to tumor progression. Researchers have found that BTLA and HVEM are abnormally expressed in various tumors and are associated with prognosis, suggesting that they may be potential targets for tumor immunotherapy. This review summarizes the molecular structures of BTLA and HVEM, immunomodulatory mechanisms, recent advances in hematologic malignancies, potential inhibitors of BTLA/HVEM interaction, and their applications in immunotherapy for hematologic malignancies.
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[Expression of BTLA/HVEM axis in hematological and prospects for immune target therapy].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
January 2025
Department of Hematology, Lanzhou University Second Hospital, Lanzhou 730000, China. *Corresponding authors, E-mail:
Article Synopsis
- BTLA is an inhibitory immune checkpoint that interacts with HVEM to regulate immune balance and maintain immune tolerance on the same cell, while also affecting different immune cells to suppress immune responses.
- Dysregulation of the BTLA/HVEM interaction can lead to impaired immune cell function, allowing tumor cells to evade immune detection and progress.
- Research indicates that BTLA and HVEM are often abnormally expressed in various tumors, making them potential targets for future immunotherapy approaches in treating hematologic malignancies.
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Front Cell Infect Microbiol
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Department of Biochemistry and Molecular Biology, School of Biology and Basic Medical Sciences, Soochow University, Suzhou, China.
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- Pulmonary tuberculosis (PTB) is a serious infectious disease, and understanding the immune response to it could aid in developing treatments for drug-resistant cases, particularly by focusing on regulatory T cells (Tregs) which suppress immune responses to the bacteria.
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J Immunol
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Department of Neurology, University of California, Irvine, Irvine, CA.
N-glycan branching is a potent and multifaceted negative regulator of proinflammatory T cell and B cell function. By promoting multivalent galectin-glycoprotein lattice formation at the cell surface, branching regulates clustering and/or endocytosis of the TCR complex (TCR+CD4/CD8), CD45, CD25, BCR, TLR2 and TLR4 to inhibit T cell and B cell activation/proliferation and proinflammatory TH1 and TH17 over TH2 and induced T regulatory cell responses. In addition, branching promotes cell surface retention of the growth inhibitory receptor CTLA-4.
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