Relative versus absolute risk of comorbidities in patients with psoriasis

Saleem, Mohamed; Kesty, Chelsea; Feldman, Steven R.

doi:10.1016/j.jaad.2016.11.037

Cited by 23 publications

(20 citation statements)

References 23 publications

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“…The three principal histological features of psoriasis are hyperplastic/thickened epidermis, elongated and increased vascularity in the dermis, and inflammatory leukocyte infiltration (5). Beyond the lesions, psoriasis is also associated with several comorbidities, such as rheumatoid arthritis, atherosclerosis, cardiovascular diseases, obesity, type 2 diabetics, Alzheimer's disease, depression, and non-melanoma skin cancer (7, 8). Increased disease burden greatly impairs the quality of life in psoriasis patients.…”

Section: Psoriasis: Etiology Immunopathogenesis and Therapiesmentioning

confidence: 99%

Type1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis

Zhang

2019

Front. Immunol.

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Psoriasis is a chronic autoimmune skin disease that can often be triggered upon skin injury, known as Koebner phenomenon. Type 1 interferons (IFNα and IFNβ), key cytokines that activate autoimmunity during viral infection, have been suggested to play an indispensable role in initiating psoriasis during skin injury. Type 1 IFN-inducible gene signature has been identified as one of the major upregulated gene signatures in psoriatic skin. Type 1 IFNs treatments often directly induce or exacerbate psoriasis, whereas blocking type 1 IFNs signaling pathway in animal models effectively inhibits the development of T cell-mediated skin inflammation and psoriasis-like inflammatory diseases. Epidermal keratinocytes (KCs) occupy the outermost position in the skin and are the first responder to skin injury. Skin injury rapidly induces IFNβ from KCs and IFNα from dermal plasmacytoid dendritic cells (pDCs) through distinct mechanisms. Host antimicrobial peptide LL37 potentiates double-stranded RNA (dsRNA) immune pathways in keratinocytes and single-stranded RNA or DNA pathways in pDCs, leading to production of distinct type 1 IFN genes. IFNβ from KC promotes dendritic cell maturation and the subsequent T cell proliferation, contributing to autoimmune activation during skin injury and psoriasis pathogenesis. Accumulating evidences have indicated an important role of this dsRNA immune pathway in psoriasis pathogenesis. Together, this review describes how skin injury induces type 1 IFNs from skin cells and how this may initiate autoimmune cascades that trigger psoriasis. Targeting keratinocytes or type 1 IFNs in combination with T cell therapy may result in more sustainable effect to treat auto-inflammatory skin diseases such as psoriasis.

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Section: Psoriasis: Etiology Immunopathogenesis and Therapiesmentioning

confidence: 99%

Type1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis

Zhang

2019

Front. Immunol.

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“…In recent years, the incidence rates of PV have consistently increased year by year [2,3]. PV has long been considered a systemic inflammatory disease [4] mediated by the cells and molecules of both the innate and adaptive immune systems [5], with the participation of keratinocytes (KCs), dendritic cells (DCs), T lymphocytes, and neutrophils causing the proliferation and differentiation of keratinocytes as well as dermal vascular proliferation and expansion. Epidemiology analyses have previously demonstrated a significant association between PV and metabolic syndrome, which includes obesity, hyperlipidemia, and diabetes [6].…”

Section: Introductionmentioning

confidence: 99%

Quantitative analysis of differentially expressed proteins in psoriasis vulgaris using tandem mass tags and parallel reaction monitoring

et al. 2020

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Background: Psoriasis vulgaris (PV) is a chronic autoimmune inflammatory disease with epidermal hyperkeratosis and parakeratosis. Methods: The study was to elucidate the pathogenesis of PV by quantitative proteomic analysis of skin lesion biopsies of PV and healthy tissues with tandem mass tags (TMTs) coupled with liquid chromatography-mass spectrometry (LC-MS)/MS. Results: A total of 4562 differentially expressed proteins (DEPs) between PV lesional tissues (n = 11) and healthy tissues (n = 11) were identified, of which 299 were upregulated and 206 were downregulated using |fold change| > 1.3 as the cutoff threshold. The Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that the DEPs were mainly enriched in the activation of immune cells (drug metabolism pathway, NOD-like pathway, and IL-17 pathway), cell proliferation (ribosomal pathway, DNA replication pathway, and base replication pathway), metabolism-related pathways (fatty acid biosynthesis and metabolism, PPAR pathway, glycerophospholipid metabolism, and cortisol synthesis and breakdown), and glandular secretion (saliva secretion, gastric acid secretion, and pancreatic fluid secretion). Thirteen DEPs that were relatively highly expressed in the drug metabolism pathway were validated with parallel reaction monitoring (PRM), of which MPO, TYMP, IMPDH2, GSTM4, and ALDH3A1 were highly expressed in PV, whereas CES1, MAOB, MGST1, and GSTT1 were less expressed in PV. Conclusions: These findings confirmed that these proteins participate in the drug metabolism-other enzyme pathways and play crucial roles in the activation and proliferation of immune cells in the pathogenesis of PV.

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“…Itch, affecting 60–96% of patients, is the primary source of discomfort, negatively impacting daily physical and mental well-being [ 12 – 14 ]. Clinical studies with ixekizumab [ 15 , 16 ], tofacitinib [ 17 ], apremilast [ 18 ], etanercept [ 19 ], and secukinumab [ 20 ] have shown a significant association of improvement of itch with a correlative improvement of the quality of life for patients. Not surprisingly, the reduction of itch and pain is strongly correlated with skin clearance [ 21 ] [ 15 ].…”

Section: Current State Of Patient Satisfactionmentioning

confidence: 99%

Clinical Goals and Barriers to Effective Psoriasis Care

Strober

Walt²,

Armstrong

et al. 2018

Dermatol Ther (Heidelb)

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Engaging global key opinion leaders, the International Psoriasis Council (IPC) held a day-long roundtable discussion with the primary purpose to discuss the treatment goals of psoriasis patients and worldwide barriers to optimal care. Setting clear expectations might ultimately encourage undertreated psoriasis patients to seek care in an era in which great gains in therapeutic efficacy have been achieved. Here, we discuss the option for early treatment of all categories of psoriasis to alleviate disease impact while emphasizing the need for more focused attention for psoriasis patients with mild and moderate forms of this autoimmune disease. In addition, we encourage policy changes to keep pace with the innovative therapies and clinical science and highlight the demand for greater understanding of treatment barriers in resource-poor countries.

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Relative versus absolute risk of comorbidities in patients with psoriasis

Cited by 23 publications

References 23 publications

Type1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis

Type1 Interferons Potential Initiating Factors Linking Skin Wounds With Psoriasis Pathogenesis

Quantitative analysis of differentially expressed proteins in psoriasis vulgaris using tandem mass tags and parallel reaction monitoring

Clinical Goals and Barriers to Effective Psoriasis Care

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