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Interleukin-17 Drives Interstitial Entrapment of Tissue Lipoproteins in Experimental Psoriasis. | LitMetric

AI Article Synopsis

  • * Researchers used a photoactivatable form of apoA-I to study how HDL moves through tissues, particularly focusing on the differences in skin and arteries between healthy mice and those with psoriasis, a condition linked to higher cardiovascular risk.
  • * The study found that psoriasis promotes the migration of certain immune cells (T cells) to the arteries, leading to collagen changes that trap lipoproteins, ultimately increasing vascular stiffness and atherosclerosis, highlighting interleukin-17's significant

Article Abstract

Lipoproteins trapped in arteries drive atherosclerosis. Extravascular low-density lipoprotein undergoes receptor uptake, whereas high-density lipoprotein (HDL) interacts with cells to acquire cholesterol and then recirculates to plasma. We developed photoactivatable apoA-I to understand how HDL passage through tissue is regulated. We focused on skin and arteries of healthy mice versus those with psoriasis, which carries cardiovascular risk in man. Our findings suggest that psoriasis-affected skin lesions program interleukin-17-producing T cells in draining lymph nodes to home to distal skin and later to arteries. There, these cells mediate thickening of the collagenous matrix, such that larger molecules including lipoproteins become entrapped. HDL transit was rescued by depleting CD4 T cells, neutralizing interleukin-17, or inhibiting lysyl oxidase that crosslinks collagen. Experimental psoriasis also increased vascular stiffness and atherosclerosis via this common pathway. Thus, interleukin-17 can reduce lipoprotein trafficking and increase vascular stiffness by, at least in part, remodeling collagen.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6365189PMC
http://dx.doi.org/10.1016/j.cmet.2018.10.006DOI Listing

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