Circulating cochlin LCCL domain binds to dying cells and enhances efferocytosis
Abstract
Clearance of dead cells by efferocytosis is a critical process for homeostasis, notably by limiting inflammation. Defective efferocytosis has been associated with autoimmune, neurodegenerative, and cardiovascular diseases, as well as chronic infections, making its regulation a potential therapeutic target. Here, we identify circulating cochlin LCCL (Limulus factor C, Cochlin, and Lgl1) domain as a regulator of efferocytosis. Using cell binding assay for recombinant cochlin LCCL domain, we establish its tropism for dead or dying cells of both immune and non-immune lineages from murine and human origins. By three independent functional assays, we demonstrate that endogenous and exogenous cochlin LCCL domain enhances macrophage efferocytosis in vitro and in vivo in lipopolysaccharide (LPS)-induced inflammation and intranasal Pseudomonas aeruginosa infection, to a similar extent as the efferocytosis promoter GAS6. Our findings provide a role of cochlin LCCL domain in the regulation of efferocytosis, alongside its already described pro-inflammatory role, as an immunomodulator for host response and homeostasis.
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BibTeX
@article{courcol2026circulating,
title = {{Circulating cochlin LCCL domain binds to dying cells and enhances efferocytosis}},
author = {Louise Courcol and Ali Hassan and Zofia Haftek-Terreau and Clara Vigneron and Ananga Ghosh and Lucie Collombet and Stefan Tholen and Gaëtan Juban and Anne-Claire Lukaszewicz and Oliver Schilling and Bénédicte F Py and Fabienne Venet},
journal = {Cell Reports},
year = {2026},
month = oct,
doi = {10.1016/j.celrep.2026.117771},
url = {https://hal.science/hal-05775966v1},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Circulating cochlin LCCL domain binds to dying cells and enhances efferocytosis
AU - Louise Courcol
AU - Ali Hassan
AU - Zofia Haftek-Terreau
AU - Clara Vigneron
AU - Ananga Ghosh
AU - Lucie Collombet
AU - Stefan Tholen
AU - Gaëtan Juban
AU - Anne-Claire Lukaszewicz
AU - Oliver Schilling
AU - Bénédicte F Py
AU - Fabienne Venet
PY - 2026
DA - 2026/10/02
JO - Cell Reports
DO - 10.1016/j.celrep.2026.117771
UR - https://hal.science/hal-05775966v1
AB - Clearance of dead cells by efferocytosis is a critical process for homeostasis, notably by limiting inflammation. Defective efferocytosis has been associated with autoimmune, neurodegenerative, and cardiovascular diseases, as well as chronic infections, making its regulation a potential therapeutic target. Here, we identify circulating cochlin LCCL (Limulus factor C, Cochlin, and Lgl1) domain as a regulator of efferocytosis. Using cell binding assay for recombinant cochlin LCCL domain, we establish its tropism for dead or dying cells of both immune and non-immune lineages from murine and human origins. By three independent functional assays, we demonstrate that endogenous and exogenous cochlin LCCL domain enhances macrophage efferocytosis in vitro and in vivo in lipopolysaccharide (LPS)-induced inflammation and intranasal Pseudomonas aeruginosa infection, to a similar extent as the efferocytosis promoter GAS6. Our findings provide a role of cochlin LCCL domain in the regulation of efferocytosis, alongside its already described pro-inflammatory role, as an immunomodulator for host response and homeostasis.
SN - 2211-1247
SN - 2211-1247
ER -