HDL in innate and adaptive immunity

During infections or acute conditions high-density lipoproteins cholesterol (HDL-C) levels decrease very rapidly and HDL particles undergo profound changes in their composition and function. These changes are associated with poor prognosis following endotoxemia or sepsis and data from genetically mo...

Full description

Bibliographic Details
Main Authors: Catapano, A., Pirillo, A., Bonacina, F., Norata, Giuseppe
Format: Journal Article
Published: 2014
Online Access:http://hdl.handle.net/20.500.11937/55745
_version_ 1848759695902244864
author Catapano, A.
Pirillo, A.
Bonacina, F.
Norata, Giuseppe
author_facet Catapano, A.
Pirillo, A.
Bonacina, F.
Norata, Giuseppe
author_sort Catapano, A.
building Curtin Institutional Repository
collection Online Access
description During infections or acute conditions high-density lipoproteins cholesterol (HDL-C) levels decrease very rapidly and HDL particles undergo profound changes in their composition and function. These changes are associated with poor prognosis following endotoxemia or sepsis and data from genetically modified animal models support a protective role for HDL. The same is true for some parasitic infections, where the key player appears to be a specific and minor component of HDL, namely apoL-1. The ability of HDL to influence cholesterol availability in lipid rafts in immune cells results in the modulation of toll-like receptors, MHC-II complex, as well as B- and T-cell receptors, while specific molecules shuttled by HDL such as sphingosine-1-phosphate (S1P) contribute to immune cells trafficking. Animal models with defects associated with HDL metabolism and/or influencing cell cholesterol efflux present features related to immune disorders. All these functions point to HDL as a platform integrating innate and adaptive immunity. The aim of this review is to provide an overview of the connection between HDL and immunity in atherosclerosis and beyond. © The Author 2014.
first_indexed 2025-11-14T10:03:59Z
format Journal Article
id curtin-20.500.11937-55745
institution Curtin University Malaysia
institution_category Local University
last_indexed 2025-11-14T10:03:59Z
publishDate 2014
recordtype eprints
repository_type Digital Repository
spelling curtin-20.500.11937-557452017-09-13T16:11:11Z HDL in innate and adaptive immunity Catapano, A. Pirillo, A. Bonacina, F. Norata, Giuseppe During infections or acute conditions high-density lipoproteins cholesterol (HDL-C) levels decrease very rapidly and HDL particles undergo profound changes in their composition and function. These changes are associated with poor prognosis following endotoxemia or sepsis and data from genetically modified animal models support a protective role for HDL. The same is true for some parasitic infections, where the key player appears to be a specific and minor component of HDL, namely apoL-1. The ability of HDL to influence cholesterol availability in lipid rafts in immune cells results in the modulation of toll-like receptors, MHC-II complex, as well as B- and T-cell receptors, while specific molecules shuttled by HDL such as sphingosine-1-phosphate (S1P) contribute to immune cells trafficking. Animal models with defects associated with HDL metabolism and/or influencing cell cholesterol efflux present features related to immune disorders. All these functions point to HDL as a platform integrating innate and adaptive immunity. The aim of this review is to provide an overview of the connection between HDL and immunity in atherosclerosis and beyond. © The Author 2014. 2014 Journal Article http://hdl.handle.net/20.500.11937/55745 10.1093/cvr/cvu150 unknown
spellingShingle Catapano, A.
Pirillo, A.
Bonacina, F.
Norata, Giuseppe
HDL in innate and adaptive immunity
title HDL in innate and adaptive immunity
title_full HDL in innate and adaptive immunity
title_fullStr HDL in innate and adaptive immunity
title_full_unstemmed HDL in innate and adaptive immunity
title_short HDL in innate and adaptive immunity
title_sort hdl in innate and adaptive immunity
url http://hdl.handle.net/20.500.11937/55745