Autoimmune diseases constitute a heterogeneous group of disorders with one common feature - the loss of immune tolerance towards autoantigens. Due to the complexity of the pathogenesis of these diseases, there are still many open questions regarding their etiology. Therefore, scientists unceasingly search for new data hoping to detect dependable biomarkers and design safe and effective treatment. The research on immune checkpoints is in line with these scientific and clinical demands. Immune checkpoints may be the key to understanding the pathogenesis of many immunological disorders. BTLA-HVEM complex, the inhibitory immune checkpoint, has recently caught scientific attention as an important regulator in different immune contexts, including autoreactivity. So far, the BTLA-HVEM complex has been mainly studied in the context of cancer, but as numerous data show, it may also be a target in the treating of autoimmune diseases. In this review, we intend to focus on the mechanisms of BTLA-HVEM interactions in immune cells and summarize the available data in the context of autoimmunity.
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| http://dx.doi.org/10.1016/j.cellimm.2022.104532 | DOI Listing |
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Distinct characteristics of BTLA/HVEM axis expression on Tregs and its impact on the expansion and attributes of Tregs in patients with active pulmonary tuberculosis.
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Department of Biochemistry and Molecular Biology, School of Biology and Basic Medical Sciences, Soochow University, Suzhou, China.
Article Synopsis
- 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.
- The study used flow cytometry to analyze Treg frequency and the expression of key immune molecules (BTLA, HVEM, PD-L1, PD-1) in PTB patients compared to healthy controls, finding an increased presence of Tregs in patients.
- Interestingly, while BTLA and HVEM levels decreased on Tregs in PTB patients, these changes suggested a complex interaction that may enhance Treg activation, with mechanisms behind this needing further investigation.
N-Glycan Branching Regulates BTLA Opposite to PD-1 to Limit T Cell Hyperactivity Induced by Branching Deficiency.
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.
View Article and Find Full Text PDFThe effect of gD-derived peptides on T cell immune response mediated by BTLA-HVEM protein complex in melanoma patients.
Front Immunol
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Department of Biomedical Chemistry, Faculty of Chemistry, University of Gdańsk, Gdańsk, Poland.
Introduction: The effector function of T cells is regulated via immune checkpoints, activating or inhibiting the immune response. The BTLA-HVEM complex, the inhibitory immune checkpoint, may act as one of the tumor immune escape mechanisms. Therefore, interfering with the binding of these proteins can prove beneficial in cancer treatment.
View Article and Find Full Text PDFTargeting BTLA with the peptide inhibitor HVEM(14-39) - A new way to restore the activity of T cells in melanoma.
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Department of Biomedical Chemistry, Faculty of Chemistry, University of Gdańsk, Poland. Electronic address:
The complex of B- and T-lymphocyte attenuator (BTLA) and herpes virus entry mediator (HVEM) plays a critical role in immune regulation and has emerged as a promising therapeutic target for cancer treatment. In this study, we investigated the potential of the peptide inhibitor HVEM(14-39) to restore peripheral T cell activity in patients with advanced melanoma. In these patients, CD8+ T cells downregulated BTLA expression and increased HVEM expression upon activation.
View Article and Find Full Text PDFThe role of the BTLA-HVEM complex in the pathogenesis of breast cancer.
Breast Cancer
May 2024
College of Health Industry, Changchun University of Architecture and Civil Engineering, Changchun, 130000, China.
Article Synopsis
- * The BTLA-HVEM complex is an important regulator of immune responses, as its interaction on T cells decreases their activation and growth.
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