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Publication

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

Cell metabolism | 2019

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.

Pubmed ID: 30415924 RIS Download

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Associated grants

Agency: NIAID NIH HHS, United States
Id: R37 AI049653
Agency: NHLBI NIH HHS, United States
Id: R01 HL127649
Agency: NIDDK NIH HHS, United States
Id: P30 DK056341
Agency: NHLBI NIH HHS, United States
Id: T32 HL007081
Agency: NIDDK NIH HHS, United States
Id: DP1 DK109668
Agency: NIAID NIH HHS, United States
Id: T32 AI007163
Agency: NHLBI NIH HHS, United States
Id: R01 HL118206
Agency: NHLBI NIH HHS, United States
Id: R01 HL112276

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