Myeloid C-type lectin receptors in host-pathogen interactions and glycan-based targeting.
Autor: | Stegmann F; Institute for Immunology, University of Veterinary Medicine Hannover, 30559 Hannover, Lower Saxony, Germany; Research Center for Emerging Infections and Zoonoses, University of Veterinary Medicine Hannover, 30559 Hannover, Lower Saxony, Germany., Lepenies B; Institute for Immunology, University of Veterinary Medicine Hannover, 30559 Hannover, Lower Saxony, Germany; Research Center for Emerging Infections and Zoonoses, University of Veterinary Medicine Hannover, 30559 Hannover, Lower Saxony, Germany. Electronic address: bernd.lepenies@tiho-hannover.de. |
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Jazyk: | angličtina |
Zdroj: | Current opinion in chemical biology [Curr Opin Chem Biol] 2024 Oct; Vol. 82, pp. 102521. Date of Electronic Publication: 2024 Aug 29. |
DOI: | 10.1016/j.cbpa.2024.102521 |
Abstrakt: | Lectin-glycan interactions play a crucial role in the immune system. An important class of lectins in the innate immune system is myeloid C-type lectin receptors (CLRs). Myeloid CLRs act as pattern recognition receptors and are predominantly expressed by myeloid cells, such as macrophages, dendritic cells, and neutrophils. In innate immunity, CLRs contribute to self/non-self discrimination. While the recognition of pathogen-associated molecular patterns (PAMPs) by CLRs may contribute to a protective immune response, CLR engagement can also be exploited by pathogens for immune evasion. Since various CLRs act as endocytic receptors and trigger distinct signaling pathways in myeloid cells, CLR targeting has proven useful for drug/antigen delivery into antigen-presenting cells and the modulation of immune responses. This review covers recent discoveries of pathogen/CLR interactions and novel approaches for CLR targeting within the period of the past two years. Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.) |
Databáze: | MEDLINE |
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