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Resident memory T cells (T RM) have been described as a non-circulating memory T cell subset that persists long-term in peripheral tissues psoriasis is one of the T RM-mediated autoimmune inflammatory skin diseases. This study suggests that NGF plays a critical role in the pathogenesis of psoriasis and that the regulatory role of NGF and its receptor system is functionally active in the early stage of developing lesions of psoriasis. Notably, the keratinocytes of patients with psoriasis produce higher levels of NGF. In addition, NGF secreted by the psoriatic keratinocytes is functionally active. After a cutaneous trauma, in a developing psoriasis lesion, keratinocyte proliferation and up-regulation of NGF in basal keratinocytes are early events and precede epidermotropism of T lymphocytes. NGF is thought to be associated with the Koebner phenomenon.
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Nerve growth factor (NGF) is a neurotrophic factor that is expressed in both the nervous system and peripheral organs. However, the mechanisms underlying the Koebner phenomenon remain to be completely elucidated. It is speculated that increased papillary dermis blood flow helps bring mediators that play a part in the pathogenesis of psoriasis. Under appropriate conditions, the Koebner phenomenon may occur, especially when there is dermal trauma with epidermal involvement. Type, site, depth, and degree of trauma may affect the pathogenesis of the Koebner phenomenon. However, psoriatic lesions are not always observed in the uninvolved skin after injuries. Radiotherapy, ultraviolet (UV) B, and even a slight skin irritation have been reported to trigger new lesions of psoriasis. In patients with psoriasis, skin lesions appear in uninvolved areas after various injuries this is known as the Koebner phenomenon. In this review, we focus on each component of these groups and discuss their effects on the development of psoriasis. The risk factors for psoriasis can be divided into two groups, namely, extrinsic and intrinsic risk factors ( Figure 1). The comorbidities included hypertension (1.1% to 27.8%), diabetes mellitus (DM) (7.0% to 13.9%), cardiovascular diseases (4.2% to 8.1%), and tonsillitis (3.5% to 5.4%). In past surveys from 1982 to 2012, the exacerbating factors for the Japanese population were observed to be stress (6.4% to 16.6%), seasonal factors (9.7% to 13.3%), infection (3.5% to 8.3%), sun exposure (1.3% to 3.5%), and β-blockers (0.9% to 2.3%). In genetically predisposed individuals, various triggering factors can elicit the disease. HLA-Cw6 is the susceptibility allele within PSORS1 it is associated with early onset and severe and unstable disease. Psoriasis susceptibility 1 (PSORS1), which lies within an approximately 220 kb segment of the major histocompatibility complex on chromosome 6p21, is a major susceptibility locus for psoriasis. Genetic factors play a significant role in the pathogenesis of psoriasis. The prevalence of psoriasis varies with the country, and psoriasis can appear at any age, suggesting that ethnicity, genetic background, and environmental factors affect the onset of psoriasis.
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Psoriasis is one of the most frequent chronic inflammatory skin diseases. Psoriasis is a chronic inflammatory skin disease characterized by sharply demarcated erythematous plaques with whitish scale. In this review, we summarize the risk factors, which can be divided into two groups (namely, extrinsic and intrinsic risk factors), responsible for the onset and exacerbation of psoriasis in order to facilitate its prevention. In addition, psoriasis may be associated with other auto-inflammatory and auto-immune diseases. Recent studies suggest that the exacerbation of psoriasis can lead to systemic inflammation and cardiovascular comorbidity. In contrast, various triggering factors can elicit the disease in genetically predisposed individuals. These biologics have dramatically changed the treatment and management of psoriasis. In the past decade, biologics targeting tumor necrosis factor-α, interleukin (IL)-23, and IL-17 have been developed and approved for the treatment of psoriasis. T cells interact with dendritic cells, macrophages, and keratinocytes, which can be mediated by their secreted cytokines. The underlying pathomechanisms involve complex interaction between the innate and adaptive immune system. Psoriasis is an immune-mediated genetic skin disease.