Topical Anthralin for Psoriasis Vulgaris: Evaluation of 70 Japanese Patients

Yamamoto, Toshiyuki; Matsuuchi, M.; Irimajiri, Junya; Otoyama, Kazunobu; Nishioka, Kiyoshi

doi:10.1111/j.1346-8138.2000.tb02212.x

Cited by 11 publications

(8 citation statements)

References 16 publications

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“… 133 Also, mast cells’ numbers decrease in psoriasis lesions after successful therapy with anthralin, psoralen plus UVA light therapy and cyclosporine. 129 , 134 , 135 …”

Section: Cellular Participants In Psoriasismentioning

confidence: 99%

Current knowledge on psoriasis and autoimmune diseases

Ayala-Fontánez¹,

Soler²,

McCormick³

2016

PTT

116

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Psoriasis is a prevalent, chronic inflammatory disease of the skin, mediated by crosstalk between epidermal keratinocytes, dermal vascular cells, and immunocytes such as antigen presenting cells (APCs) and T cells. Exclusive cellular “responsibility” for the induction and maintenance of psoriatic plaques has not been clearly defined. Increased proliferation of keratinocytes and endothelial cells in conjunction with APC/T cell/monocyte/macrophage inflammation leads to the distinct epidermal and vascular hyperplasia that is characteristic of lesional psoriatic skin. Despite the identification of numerous susceptibility loci, no single genetic determinant has been identified as responsible for the induction of psoriasis. Thus, numerous other triggers of disease, such as environmental, microbial and complex cellular interactions must also be considered as participants in the development of this multifactorial disease. Recent advances in therapeutics, especially systemic so-called “biologics” have provided new hope for identifying the critical cellular targets that drive psoriasis pathogenesis. Recent recognition of the numerous co-morbidities and other autoimmune disorders associated with psoriasis, including inflammatory bowel disease, multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus suggest common signaling elements and cellular mediators may direct disease pathogenesis. In this review, we discuss common cellular pathways and participants that mediate psoriasis and other autoimmune disorders that share these cellular signaling pathways.

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“… 133 Also, mast cells’ numbers decrease in psoriasis lesions after successful therapy with anthralin, psoralen plus UVA light therapy and cyclosporine. 129 , 134 , 135 …”

Section: Cellular Participants In Psoriasismentioning

confidence: 99%

Current knowledge on psoriasis and autoimmune diseases

Ayala-Fontánez¹,

Soler²,

McCormick³

2016

PTT

116

View full text Add to dashboard Cite

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“…Mast cells frequently degranulate in early eruptive and recurring psoriasis lesions and have been described as ‘ghost cells’ (22-24). Interestingly, mast cell numbers are decreased in psoriasis lesions after successful treatment with anthralin, PUVA, or cyclosporine (25-27). Neutrophils are also enriched in psoriasis lesions, especially in the epidermis where they aggregate in Munro’s microabscesses (MM) in the stratum corneum and spongiform pustules of Kogoj (SPK) in the stratum spinosum (28).…”

Section: Introductionmentioning

confidence: 99%

Mast Cells and Neutrophils Release IL-17 through Extracellular Trap Formation in Psoriasis

Lin

Rubin

Khandpur

et al. 2011

The Journal of Immunology

785

704

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IL-17 and IL-23 are absolutely central to psoriasis pathogenesis as drugs targeting either cytokine are highly effective treatments for this disease. The efficacy of these drugs has been attributed to blocking the function of IL-17-producing T cells and their IL-23-induced expansion. However, we demonstrate that mast cells and neutrophils, not T cells, are the predominant cell types that contain IL-17 in human skin. IL-17+ mast cells and neutrophils are found at higher densities than IL-17+ T cells in psoriasis lesions and frequently release IL-17 in the process of forming specialized structures called extracellular traps (MCETs and NETs, respectively). Furthermore, we find that IL-23 and IL-1β can induce MCET formation and degranulation of human mast cells. Release of IL-17 from innate immune cells may be central to the pathogenesis of psoriasis, representing a fundamental mechanism by which the IL-23-IL-17 axis mediates host defense and autoimmunity.

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“…An excessive 54 activation of the innate immunity is often the result of a chronic inflam-55 matory process in the organism. Exogenous and endogenous factors 56 may induce this process. Exogenous factors include the most conserved 57 structures of microorganisms, i.e.…”

mentioning

confidence: 98%