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Psoriasis is a chronic inflammatory skin disease that may affect any body area, including sensitive sites such as face, nails, scalp, hands, palms, feet, and genitals. Although less frequent, severe forms of either geographic or fissured tongue accounting for psoriasis manifestations can also occur. The involvement of these sites may lead to a marked impairment of quality of life, interfering with work productivity, leisure, and social activities.1 According to current guidelines, the therapeutic approach for psoriasis of these particular sites, although localized and classified as mild or mild-to-moderate, might require systemic therapies, including biologics.2

Visual Abstract, Highlights • LDGs are a subset of neutrophils that were elevated in psoriasis and associated with the severity of disease. • In psoriasis, LDGs associated with noncalcified coronary plaque burden beyond cardiovascular risk factors and in vitro, induced endothelial cell damage. • Compared to normal-density granulocyte neutrophils, platelet-associated biological pathways were upregulated in LDGs, suggesting enhanced platelet adherence to the LDG surface. • LDGs co-localized with platelets in circulation, and the LDG-platelet interaction associated more strongly with non-calcified coronary burden by coronary CTA compared to LDGs alone., Summary Psoriasis is an inflammatory skin disease associated with increased cardiovascular risk and serves as a reliable model to study inflammatory atherogenesis. Because neutrophils are implicated in atherosclerosis development, this study reports that the interaction among low-density granulocytes, a subset of neutrophils, and platelets is associated with a noncalcified coronary plaque burden assessed by coronary computed tomography angiography. Because early atherosclerotic noncalcified burden can lead to fatal myocardial infarction, the low-density granulocyte−platelet interaction may play a crucial target for clinical intervention.

Objective To investigate the relationship between psoriasis and interstitial pneumonia (IP). Patients and Methods We analyzed the clinical data of patients with psoriasis treated with biologic agents from June 1, 2008, to June 30, 2017, retrospectively. Chest computed tomography was performed in 392 patients before treatment. The clinical characteristics and radiographic findings of these patients were evaluated. Results Of the 392 patients with psoriasis, IP was detected in 8 patients (2%). Bilateral ground-glass and/or irregular linear (reticular) opacity in the lower lung zone was the most common chest computed tomography finding. Five of the 8 patients with IP were treated with anti–interleukin (IL) 12/IL-23 or IL-17 antibodies, leading to decreased or stable IP activity. Conclusion Interstitial pneumonia was detected in 2% of patients with psoriasis who needed systemic treatments. Ground-glass and/or irregular linear (reticular) opacity in the bilateral lower lobes was characteristic of IP with psoriasis. The IL-23/IL-17 axis may play important roles in the pathogenesis of IP in psoriasis.

Contains fulltext : 169829.pdf (Publisher’s version ) (Open Access) Elucidating the poorly defined mechanisms by which inflammatory lesions are spatially restricted in vivo is of critical importance in understanding skin disease. Chemokines are the principal regulators of leukocyte migration and are essential in the initiation and maintenance of inflammation. The membrane-bound psoriasis-associated atypical chemokine receptor 2 (ACKR2) binds, internalizes and degrades most proinflammatory CC-chemokines. Here we investigate the role of ACKR2 in limiting the spread of cutaneous psoriasiform inflammation to sites that are remote from the primary lesion. Circulating factors capable of regulating ACKR2 function at remote sites were identified and examined using a combination of clinical samples, relevant primary human cell cultures, in vitro migration assays, and the imiquimod-induced model of psoriasiform skin inflammation. Localized inflammation and IFN-gamma together up-regulate ACKR2 in remote tissues, protecting them from the spread of inflammation. ACKR2 controls inflammatory T-cell chemotaxis and positioning within the skin, preventing an epidermal influx that is associated with lesion development. Our results have important implications for our understanding of how spatial restriction is imposed on the spread of inflammatory lesions and highlight systemic ACKR2 induction as a therapeutic strategy in the treatment and prevention of psoriasis and potentially a broad range of other immune-mediated diseases.