2026-04-28T21:35:05Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/96092024-09-27T09:30:58Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
del Fresno, Carlos
author
Cueto, Francisco J.
author
Sancho, David
funder
Asociación Española Contra el Cáncer
funder
Fundación La Caixa
funder
Unión Europea. Comisión Europea
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Comunidad de Madrid (España)
funder
Instituto de Salud Carlos III
funder
Fondation ACTERIA (Acting on European Research in Immunology and Allergology)
funder
Atresmedia
funder
Fundación La Marató TV3
funder
Fundación ProCNIC
2020-04-17T13:58:02Z
2020-04-17T13:58:02Z
2020-01-24
Curr Top Microbiol Immunol. 2020, Jan 24
0070-217X
http://hdl.handle.net/20.500.12105/9609
31974758
10.1007/82_2019_194
Current topics in microbiology and immunology
After both sterile and infectious insults, damage is inflicted on tissues leading to accidental or programmed cell death. In addition, events of programmed cell death also take place under homeostatic conditions, such as in embryo development or in the turnover of hematopoietic cells. Mammalian tissues are seeded with myeloid immune cells, which harbor a plethora of receptors that allow the detection of cell death, modulating immune responses. The myeloid C-type lectin receptors (CLRs) are one of the most prominent families of receptors involved in tailoring immunity after sensing dead cells. In this chapter, we will cover a diversity of signals arising from different forms of cell death and how they are recognized by myeloid CLRs. We will also explore how myeloid cells develop their sentinel function, exploring how some of these CLRs identify cell death and the type of responses triggered thereof. In particular, we will focus on DNGR-1 (CLEC9A), Mincle (CLEC4E), CLL-1 (CLEC12A), LOX-1 (OLR1), CD301 (CLEC10A) and DEC-205 (LY75) as paradigmatic death-sensing CLRs expressed by myeloid cells. The molecular processes triggered after cell death recognition by myeloid CLRs contribute to the regulation of immune responses in pathologies associated with tissue damage, such as infection, autoimmunity and cancer. A better understanding of these processes may help to improve the current approaches for therapeutic intervention.
eng
C-type lectin receptors
Cell death
Dendritic cells
Macrophages
Myeloid
Sensing Tissue Damage by Myeloid C-Type Lectin Receptors
journal article
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SensingTissueDamageMyeloid_2020.pdf
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SensingTissueDamageMyeloid_2020.pdf.txt