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Immune synapses, which were initially discovered at the interface between antigen-presenting cells (APCs) and T cells, are special structures formed at the contact site between antigen-presenting cells and immune cells and constitute the structural basis for immune cells to kill tumours and synthesise antibodies. Their structures are very similar to those of neural synapses in the nervous system, and they contain different functional structural regions. With the development of cell visualization research, scientists have increasingly conducted in-depth research on immune synapses. At present, it is known that T cells, B cells, and NK cells can form different immune synapses with target cells. Immune synapses formed by different cell subsets as well as CAR-T cells have their own characteristics, mainly in terms of their structure, formation process and regulatory mechanism. Therefore, how to enhance immune cell killing function by enhancing immune synaptic function has long been a research hotspot. At present, the killing function of immune cells can be enhanced by influencing the signalling molecules of immune synapses and the cell microenvironment and modifying the structure of immune synapses. Through a review of the factors affecting immune synapses, we can better explore the target for enhancing immune system function.
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http://dx.doi.org/10.1016/j.canlet.2025.217542 | DOI Listing |
Front Immunol
September 2025
Immunocore Ltd., Abingdon, United Kingdom.
Background: The programmed cell death protein 1 (PDCD1 or PD-1) is a key regulatory immune checkpoint and a major target for therapeutic intervention. In oncology, antibodies blocking the PD-1 pathway are used to activate immune cells to promote anti tumour immunity while in immune-mediated inflammatory diseases, PD-1 agonist molecules have the potential to achieve immune suppression. NK cells are a specialised population of innate lymphocytes able to recognize a large range of distressed cells including damaged tissues in autoimmune and inflammatory conditions.
View Article and Find Full Text PDFBMB Rep
September 2025
Department of Microbiology and Immunology, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea; Brain Korea 21 PLUS Project for Medical Sciences, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea; Institute for Immunology and Immunological Diseases, Yonsei Uni
B cell tolerance is critical for preventing autoimmunity, yet the mechanisms by which B cells discriminate self from non-self antigens remain incompletely understood. While early findings emphasize the role of classical antigen-mediated BCR signaling strength by varying antigen formats, emerging evidence highlights the importance of mechanical cues during antigen recognition. This review explores how mechanosensitive ion channels, particularly Piezo1, contribute to B cell activation and tolerance by integrating physical forces at the immune synapse.
View Article and Find Full Text PDFCell Rep
September 2025
Weill Cornell Medicine, New York, NY 10065, USA. Electronic address:
An adverse gestational environment is a risk factor for the development of psychiatric disorders. Although studies have implicated modifications in neuronal DNA and chromatin, how these changes come about and lead to abnormal behaviors is not known. We sought to identify persistent DNA/chromatin and transcriptomic signatures induced by a proinflammatory gestational environment in the ventral dentate gyrus (vDG), a hippocampal region linked to anxiety.
View Article and Find Full Text PDFT cell activation is characterized by rapid reorganization of the actin cytoskeleton and cell spreading on the antigen presenting cell. The T cell nucleus occupies a large fraction of the cell volume, and its mechanical properties are likely to act as a key determinant of activation. However, the contribution of nuclear mechanics to T cell spreading and activation is not well understood.
View Article and Find Full Text PDFACS Cent Sci
August 2025
Department of Immunology and Microbiology, The Scripps Research Institute, La Jolla, California 92037, United States.
Immune therapies targeting the PD1 axis have transformed outcomes in cancer treatment by enhancing T cell-mediated immune responses. However, many tumors evade immune clearance through orthogonal escape mechanisms. Excessive production of immunosuppressive sialic acid-containing glycans (sialoglycans) can impair immune surveillance by recruiting inhibitory Siglecs to the immune synapse where, like PD1, they act as checkpoints for cell activation.
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