Psoriatic arthritis (PsA) is a highly heterogeneous systemic autoimmune disease, characterized by severe manifestations that involve psoriasis, defined as the presence of erythematous, scaly, well-demarked plaques, with thickening of skin associated to musculoskeletal illness as spondylitis, enthesitis, or peripheral arthritis.¹ The PsA is classified into spondyloarthropathies, usually negative for rheumatoid factor.² Currently, it is identified by two clinical subtypes: first, oligoarticular PsA that can evolve conforming severity of disease, antinuclear antibodies’ positivity, uveitis, and dactylitis; second, polyarticular PsA that may present enthesitis, nail pitting, onycholysis, and spondylitis.³ The worldwide prevalence of PsA is highly heterogeneous; however, in Mexico, it was estimated in 0.02%⁴ with a 1:1 ratio between males and females. Likewise, several comorbidities have been associated with PsA as obesity, metabolic syndrome, and cardiovascular disease.⁵ The etiology of PsA is still elusive, but several factors including the environment, genetic factors, and the immune dysfunction are associated with the development of this disease.³ In the pathogenesis of PsA, immune dysfunction is the main player in the development of pathological manifestations in the skin, enthesis, and synovium, driven by distinct T helper (Th) cell subsets.⁶ Particularly, a strong deregulation of Th17 cytokine profile has been implicated with an increase in epidermal and joint damage in PsA. On the other hand, other cytokines such as interleukin (IL)-31 have been implicated in skin inflammatory diseases such as atopic dermatitis,⁷ but there are no existing reports regarding PsA. IL-31 is a cytokine produced mainly by the immune system cells such as Th2 and mast cells, and it has been demonstrated that interferon γ (IFNγ) and the cathelicidin LL-37 can upregulate IL-31 expression.⁸ IL-31 has been shown to induce the secretion of cytokines such as IL-6, IL-8, and IL-32 as well as chemokines and matrix metalloproteinases (MMPs) in diseases involving chronic skin inflammation, suggesting a proinflammatory role.⁸ Based on this knowledge, this study was focused on the evaluation of IL-31 and Th17 cytokine profile serum levels in PsA, as well as the retinoic acid-related orphan receptor C (RORC) gene expression, which represents the main transcription factor associated to Th17 cell differentiation in autoimmune diseases.^9,10

中文翻译：

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IL-31在银屑病关节炎中的潜在炎症作用：与Th17细胞因子谱的相关性

银屑病关节炎（PsA）是高度异质的全身性自身免疫性疾病，其特征是涉及牛皮癣的严重表现，定义为存在红斑，鳞片，标记斑块，与肌肉骨骼疾病相关的皮肤增厚，如脊椎炎，脑炎或周围神经关节炎。¹ PsA分为脊椎关节病，通常类风湿因子阴性。²目前，它可以通过两种临床亚型来识别：第一，可发展为符合疾病严重程度的抗关节炎PsA，抗核抗体的阳性，葡萄膜炎和乳腺炎；第二，多关节PsA可能会出现皮炎，指甲凹陷，强直性溶解和脊柱炎。³PsA在全球范围内普遍存在异质性。然而，在墨西哥，估计为0.02％⁴，男女之比为1：1。同样，几种合并症也与肥胖，代谢综合征和心血管疾病有关。⁵ PsA的病因仍然难以捉摸，但包括环境，遗传因素和免疫功能障碍在内的一些因素与该疾病的发展有关。³在PsA的发病机理中，免疫功能障碍是由独特的T辅助（Th）细胞亚群驱动的皮肤，上皮和滑膜病理表现发展的主要因素。⁶特别是，Th17细胞因子谱的强烈失调与PsA中表皮和关节损伤的增加有关。另一方面，其他细胞因子如白介素（IL）-31也与特应性皮炎等皮肤炎性疾病有关[ ^7]，但目前尚无关于PsA的报道。IL-31是主要由免疫系统细胞（例如Th2和肥大细胞）产生的细胞因子，已证明干扰素γ（IFNγ）和cathelicidin LL-37可以上调IL-31的表达。⁸ IL-31已显示出在涉及慢性皮肤炎症的疾病中诱导细胞因子（例如IL-6，IL-8和IL-32以及趋化因子和基质金属蛋白酶（MMP））的分泌，提示其具有促炎作用。⁸基于此知识，本研究侧重于评估PsA中IL-31和Th17细胞因子谱的血清水平，以及视黄酸相关的孤儿受体C（RORC）基因表达，其代表与自身免疫性疾病中Th17细胞的分化。^9,10