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Comparison between guttate and plaque psoriasis in terms of serum inflammatory cytokines and antimicrobial peptides

机译:血清炎性细胞因子和抗微生物肽方面的牙龈和斑块牛皮癣的比较

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摘要

Psoriasis is a chronic inflammatory skin disease, and immunological disorder plays a crucial role in the pathogenesis of psoriasis. Antimicrobial peptides (AMPs), including cathelicidin (LL-37) and human beta-defensin (HBD)-3, are not only the basis of innate immunity but also a bridge to activate adaptive immunity. In the immune response, several inflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-6, IL-10, IL-17, IL-22, and IL-23, are involved in the occurrence and development of psoriasis.[1] Guttate psoriasis was known to have a better prognosis than other types of psoriasis with a rapid regression and a longer remission period. However, 33.0% to 68.3% of guttate psoriasis subsequently develops into chronic plaque psoriasis during the follow-up period of at least 1 or 10 years.[2] However, the association of pathogenesis between guttate and plaque psoriasis is not clear, and most studies only focus on inflammatory cytokine changes in plaque psoriasis rather than in guttate psoriasis. This study aimed to compare the levels of serum inflammatory cytokines and AMPs of the variants (plaque vs. guttate) of psoriasis vulgaris, specifically some potential treatment targets, and to reveal the pathogenesis in different clinical manifestations.
机译:牛皮癣是一种慢性炎症皮肤病,免疫疾病在牛皮癣的发病机制中起着至关重要的作用。抗微生物肽(AMPS),包括Cathelicidin(LL-37)和人β - Defensin(HBD)-3,不仅是先天免疫的基础,而且是激活适应性免疫的桥梁。在免疫应答中,几种炎症细胞因子,包括肿瘤坏死因子-α,白细胞介素(IL)-6,IL-10,IL-17,IL-22和IL-23参与牛皮癣的发生和发育。 [1]已知牙龈牛皮癣具有比其他类型的牛皮癣更好的预后,并且缓解期更长。然而,33.0%至68.3%的肠道牛皮癣随后在短期期间在至少1或10年的后续期间发展到慢性斑块牛皮癣中。[2]然而,牙龈和斑块牛皮癣之间发病机制的关联尚不清楚,大多数研究只关注斑块牛皮癣的炎症细胞因子而不是牙龈牛皮癣。本研究旨在比较牛皮癣的血清炎性细胞因子和AMPS的血清炎性细胞因子和AMPS,特别是一些潜在的治疗靶点,并揭示不同临床表现的发病机制。

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