Benjamin Lockshin, MD, Yevgeniy Balagula, MD, Joseph F

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Presentation transcript:

Interleukin 17, inflammation, and cardiovascular risk in patients with psoriasis Benjamin Lockshin, MD, Yevgeniy Balagula, MD, Joseph F. Merola, MD, MMSc Journal of the American Academy of Dermatology Volume 79, Issue 2, Pages 345-352 (August 2018) DOI: 10.1016/j.jaad.2018.02.040 Copyright © 2018 American Academy of Dermatology, Inc. Terms and Conditions

Fig 1 Psoriasis and atherosclerosis have similar underlying immunologic mechanisms.20 In psoriasis (left), myeloid dendritic cells secrete interleukin (IL) 12 and IL-23, which results in T-cell differentiation into type 1 helper T (Th1) and type 17 helper T (Th17) cell subtypes. Th1 cells in psoriatic lesions secrete tumor necrosis factor-α (TNF-α) and interferon gamma (IFN-γ), leading to keratinocyte activation and expression of adhesion molecules, including intercellular adhesion molecule 1 and keratinocyte proliferation. Th17 cells secrete IL-17 and IL-22, which promote both keratinocyte proliferation and intralesional angiogenesis. Decreased levels of regulatory T cells (Tregs) lead to altered levels of transforming growth factor-β, which promotes further Th1 and Th17 cell activation. In atherosclerosis (right), endothelial activation at sites of nascent arterial plaque promotes monocyte and lymphocyte extravasation and subsequent macrophage and dendritic cell elaboration of IL-12 and IL-23. Differentiated Th1 cells promote further atherosclerotic plaque growth, whereas Th17 cells promote intraplaque neoangiogensis and intraplaque hemorrhage. Increased levels of intraplaque IL-17 may lead to further weakening of the fibrous cap, with subsequent plaque rupture and myocardial infarction. (Adapted with permission from Armstrong AW, Voyles SV, Armstrong EJ, Fuller EN, Rutledge JC. Exp Dermatol. 2011;20:544-549.) Journal of the American Academy of Dermatology 2018 79, 345-352DOI: (10.1016/j.jaad.2018.02.040) Copyright © 2018 American Academy of Dermatology, Inc. Terms and Conditions