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Kong, Y., Wang, Y., & Wu, X. (2020). Storm of soluble immune checkpoints associated with disease severity of COVID-19. Signal Transduction and Targeted Therapy, 5(192), 1–3. Added by: Dr. Enrique Feoli (16/10/2020, 19:11) Last edited by: Dr. Enrique Feoli (03/01/2026, 13:15) |
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| Resource type: Journal Article DOI: 10.1038/s41392-020-00308-2 ID no. (ISBN etc.): 2059-3635 BibTeX citation key: Kong2020 View all bibliographic details  |
Categories: General Creators: Kong, Wang, Wu Collection: Signal Transduction and Targeted Therapy |
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Immune checkpoints (also named co-inhibitory receptors) have evolved as regulators of the host’s protective immune responses to prevent the destruction of inflamed tissues. Activation of the immune system following pathogen encounter has to be counteracted to guarantee the resolution of inflammation without inflicting tissue damage. One mechanism to achieve this goal following immune cell activation is through modulation of the expression of co-inhibitory receptors on the cell surface of lymphocytes, such as programmed cell death protein-1 (PD-1), B and T lymphocyte attenuator (BTLA), CD160, T cell immunoreceptor with Ig and ITIM domains (TIGIT), T cell immunoglobulin and mucin domain 3 (TIM-3), 2B4 (CD244), a member of the signaling lymphocyte-activation molecule (SLAM/CD150), lymphocyte activation gene 3 (LAG-3), or cytotoxic T cell associated protein 4 (CTLA4) on immune cells. Ligand binding to these co-inhibitory receptors, e.g. programmed cell death ligand 1 (PD-L1) or 2 (PD-L2), major histocompatibility complex II (MHC-II)/LSECTin, phosphatidylserine (PtdSer), high mobility group protein B1 (HMGB1), herpes virus entry mediator (HVEM), CD155/CD122, carcinoembryonic antigen-related cell adhesion molecule (CEACAM), CD48, or CD80/86 inhibits T cell function and modulates the course of the immune response. When an antigenic stimulus is present persistently in chronic inflammation, responsive cells become exhausted or die by apoptosis. Antigen-presenting cells and stromal cells express ligands for co-inhibitory receptors to prevent damage induced by T cell cytotoxic responses. This T cell subpopulation is essential to defend the host against virus-infected cells and tumor cells. Considering their mode of activation by antigens presented via the MHC class I complex, CD8+ T lymphocytes are consequently also major players in organ transplant rejection and autoimmune diseases. Therefore, the fine-tuned regulation of expression of co-inhibitory receptors as well as their corresponding ligands is a prerequisite for normal tissue homeostasis. Although being established as putative targets in anti-tumor therapy, its regulation remains elusive in inflammatory processes, in which a deeper knowledge may help us to design more effective strategies to treat these inflammatory processes.
Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |