Psoriasis and Antimicrobial Peptides

Takahashi, Toshiya; Yamasaki, Kenshi

doi:10.3390/ijms21186791

Cited by 82 publications

(72 citation statements)

References 122 publications

(169 reference statements)

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“…40 AMPs such as β-defensin, S100, and cathelicidin are secreted and activate the innate immune system. 41 AMPs enhance the binding of damageassociated molecular patterns such as self-DNA and self-RNA, which are released by microinjuries or scratches to their receptors, and promote the secretion of IFN from activated plasmacytoid dendritic cells and keratinocytes to promote inflammation in psoriasis. This process may be involved in the mechanism underlying the Köbner phenomenon in psoriasis.…”

Section: G Ene S and Dang Er S I G Nal Smentioning

confidence: 99%

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Pathophysiology of psoriasis: A review

Yamanaka

Yamamoto

Honda

2021

The Journal of Dermatology

101

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Psoriasis is a complex chronic inflammatory skin disease caused by the dynamic interplay between multiple genetic risk foci, environmental risk factors, and excessive immunological abnormalities. Psoriasis affects approximately 2% of the population worldwide, and dramatic advances have been achieved in the understanding and treatment options for psoriasis. Recent progress in biological therapies has revealed the fundamental roles of tumor necrosis factor‐α, interleukin (IL)‐23p19, and the IL‐17A axis together with skin‐resident immune cells and major signal transduction pathways in the pathogenesis of psoriasis. In addition to IL‐17‐producing T helper17 cells, innate lymphoid cell (ILC)3 induces psoriasis rashes directly without T‐cell/antigen interaction in response to the released antimicrobial peptides from activated keratinocytes and inflammatory cytokines. ILC3 typically expresses retinoic acid receptor‐related orphan receptor gamma t in the nucleus, matures in the presence of IL‐7 and IL‐23, and produces IL‐17 and IL‐22. The number of ILC3s is increased in the blood, psoriasis rash, and even in nonrash areas of psoriatic skin. Psoriasis is significantly associated with cardiovascular disease, metabolic syndrome, and inflammatory disorders, particularly the severe type. The similarity of enterobacteria in the psoriasis gut to that in diabetic patients may be related to its pathogenesis. In the current review, we focus on the pathophysiology of psoriasis in the accelerated immunological inflammatory loop, danger signal from keratinocytes, and cytokines, particularly IL‐17 and IL‐23p19. In addition, pathophysiological speculation with regard to morphology has been supplemented. Finally, the differences and similarities between psoriasis and atopic dermatitis are discussed.

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Section: G Ene S and Dang Er S I G Nal Smentioning

confidence: 99%

“…This process may be involved in the mechanism underlying the Köbner phenomenon in psoriasis. 41 AMPs also enhance the production of some type 3 and type 1 cytokines, and modulate receptors and cellular signaling in psoriasis. Neutrophil extracellular traps, complexes of self-DNA and LL-37, induce Th17.…”

Section: G Ene S and Dang Er S I G Nal Smentioning

confidence: 99%

Pathophysiology of psoriasis: A review

Yamanaka

Yamamoto

Honda

2021

The Journal of Dermatology

101

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“…Excessive levels of citrullinated peptides subsequently induce the production of anti-citrullinated peptide antibody (ACPA), a critical autoantibody involved in the pathogenesis of inflammatory diseases, such as RA synovitis (52). However, excessive citrullination of peptides is unlikely to increase the risk of psoriasis, as ACPA plays no role in the pathogenesis of this inflammatory skin disease (53). An informative analysis would be to determine whether patients with psoriasis and periodontitis have a risk of developing psoriatic arthritis compared with the general population with psoriasis (54).…”

Section: Other Bacterial Agentsmentioning

confidence: 99%

Infection‑provoked psoriasis: Induced or aggravated (Review)

et al. 2021

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Psoriasis is a common chronic, immune-mediated, inflammatory skin disorder, with a reported prevalence of 0.0-2.1% among children and 0.91-8.50% among adults, worldwide. Psoriasis is induced by several environmental factors, including infection, alcohol consumption, drugs, trauma, acute withdrawal of systemic or potent topical corticosteroids, body mass index and endocrine disorders. Increasing evidence suggest that a variety of microorganisms play key roles in the induction and exacerbation of psoriasis. Pathogens, such as streptococci and staphylococci are considered causal factors, presumably via superantigen activation of skin-seeking T cells. In addition, fungal pathogens, such as Candida and Malassezia, and viral agents, such as human immunodeficiency virus, hepatitis C virus infection and human papillomavirus, are also closely associated with psoriasis. Recently, several types of pathogens, such as Helicobacter pylori infection, Zika virus and scabies, have been reported to potentially trigger psoriasis. The present review discusses the underlying molecular mechanisms by which these infections influence psoriasis to provide a better understanding of the pathogenesis of psoriasis.

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“…1,4,18,19 In the initiation phase, plasmacytoid dendritic cells (DCs) that are activated by a complex of antimicrobial peptide (AMP) and self-nucleotide derived from injured keratinocytes via Toll-like receptors (TLRs) release a large amount of interferon (IFN)-α, which stimulates myeloid (conventional) DCs. 20,21 These activated DCs produce tumor necrosis factor (TNF) and IL-23, which both help maintain an immune response. TNF potentiates DCs by themselves and accelerates the inflammatory response by various immune cells, 1,22 whereas IL-23 significantly fortifies the pathogenic potential of Th17 cells, which are differentiated from naive CD4 + T cells in the presence of TGF-β, IL-21, and IL-6.…”

Section: Introductionmentioning

confidence: 99%

Psoriasis: Recent progress in molecular‐targeted therapies

Honma

Hayashi

2021

The Journal of Dermatology

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Psoriasis is a multifactorial recalcitrant inflammatory skin disease characterized by bothersome scaly reddish plaques especially on frequently chafed body parts, such as the extensor sites of the extremities and scalp. Nonetheless, through recent advance in molecular-targeted therapies including biologics and small-molecule inhibitors, even the severest symptoms of psoriasis and its comorbidities, such as psoriatic arthritis, can be excellently treated. The superb clinical effects lead to not only remarkable alleviation of symptoms but also a deep understanding of patients' impaired "quality of life" caused by this disease. Along with the development of novel treatment options targeting various specific molecules, such as proinflammatory cytokines and signal transduction-associated molecules, clinicians have thoroughly understood the molecular mechanism of psoriasis, and discovered that the IL-23/IL-17 axis mainly depending on Th17 cell function is a crucial pathogenesis of this disease. Accumulation of knowledge about the working mechanism and clinical effect of molecular-targeted therapies is indispensable for clinicians to establish a more refined therapeutic strategy for treating psoriasis.

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Psoriasis and Antimicrobial Peptides

Cited by 82 publications

References 122 publications

Pathophysiology of psoriasis: A review

Pathophysiology of psoriasis: A review

Infection‑provoked psoriasis: Induced or aggravated (Review)

Psoriasis: Recent progress in molecular‐targeted therapies

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