调节性T淋巴细胞和Th17细胞与银屑病的研究进展

银屑病是一种与T淋巴细胞相关的自身免疫性疾病,新近研究发现,除了与Th1细胞有关外,调节性T淋巴细胞尤其叉头/翅膀状螺旋转录因子诱导表达的调节性T细胞和Th17细胞在银屑病的发病过程中起着非常重要的作用。其中,叉头/翅膀状螺旋转录因子（＋）调节性T细胞平衡免疫抑制和免疫激活的转换在银屑病加重方面起到关键作用,Th17细胞分泌的细胞因子IL-17A、IL-17F、IL-22、IL-23、IL-36及肿瘤坏死因子α等在皮肤疾病发生发展中起到重要的作用。银屑病是由调节性T细胞和Th17细胞等多种免疫细胞和细胞因子共同参与的疾病。     

IL-23/IL-17/IL-36免疫环路在银屑病发病和治疗中的作用研究进展

银屑病是一种由免疫介导的慢性炎症性皮肤病,发病机理复杂,不易根治。除先天遗传性的因素外,银屑病的发病因素主要是获得性免疫系统及先天性免疫系统的功能紊乱。由各类免疫细胞调控形成的细胞因子免疫环路在银屑病发生和发展中发挥重要作用,其中IL-23/IL-17/IL-36免疫环路近年来备受关注。本文从树突状细胞活化与免疫失衡、树突状细胞源性的IL-23与Th17细胞分化、Th17细胞源性的IL-17与银屑病皮肤炎症、角质形成细胞源性的IL-36与正反馈环形成4个环节综述了IL-23/IL-17/IL-36免疫环路在银屑病发病和治疗中的研究进展。并从IL-23相关抑制剂、IL-17相关抑制剂及IL-36相关抑制剂3个方面分析了国内外IL-23/IL-17/IL-36免疫环路的靶向药物研究现状。最后提出同时针对IL-23/IL-17/IL-36免疫环路中的多靶点干预可能是下一代生物制剂开发的热点。为银屑病的发病机制研究及相关药物开发提供参考。     

银屑病中免疫细胞和细胞因子的作用

银屑病是一种与T淋巴细胞相关的自身免疫性疾病,新近研究发现除与Th1细胞有关外,Th17细胞及其相关的细胞因子在银屑病发病中也起重要的作用.T淋巴细胞的活化和分化需要抗原提呈细胞参与,肥大细胞活化后释放的细胞因子也参与银屑病发病.因此,银屑病是由多种免疫细胞和细胞因子共同参与的疾病.阐明银屑病发病的免疫机制可为银屑病治疗开辟新疗法提供理论依据.     

与银屑病相关的T辅助细胞研究进展

银屑病是一种由多种免疫细胞和细胞因子介导参与的慢性炎症性免疫性疾病。关于银屑病的确切发病机制尚未阐明,研究发现可能与Th1、Th2、Th17、调节性T淋巴细胞(Treg)细胞、Th22细胞及Th9细胞的异常活化并释放大量细胞因子有关。该文围绕这些免疫细胞及其相关细胞因子主要从近年所发现的Th细胞亚群及其相关细胞因子角度综述了近年来与银屑病T辅助细胞的实验研究进展,阐述各个辅助细胞及相关细胞因子在银屑病发病过程中的作用及关联机制,以期能帮助笔者更深入地了解银屑病的发病机制并为今后的实验研究提供依据。     

Th17细胞与银屑病

银屑病是一种Th1细胞免疫反应介导的慢性炎症性皮肤病.近年发现一种新型的CD4+效应性T细胞--Th17细胞,不同于Th1和Th2细胞,特异性产生IL-17,在许多既往归类于Th1介导的慢性炎症性疾病中(包括银屑病)发挥重要作用.文中将介绍Th17细胞免疫反应在银屑病发病中的作用,同时介绍其在目前银屑病治疗方法中的意义和在新的潜在治疗靶位中的前景.     

Th22细胞及其细胞因子在银屑病发病机制中的作用

银屑病是一种由T细胞介导的疾病,以表皮过度增殖、角质形成细胞异常分化伴血管增生及皮损处免疫细胞浸润为特征.近来发现了一群独立于Th1、Th2及Th17细胞的新型CD4+记忆性T细胞--Th22细胞,其在银屑病等一些炎症性皮肤病中不同程度升高,使免疫调节机制进一步完善,通过了解其作用机理或许可开展将其作为一个治疗银屑病的新型靶点的研究.本文就Th22细胞及其细胞因子在银屑病中的作用机制进行综述.     

靶向生物制剂治疗银屑病的免疫学机制和应用

<正>银屑病是多基因遗传背景下的自身免疫紊乱性疾病,其发病主要与T细胞介导的免疫有关。目前已知参与银屑病发病的T细胞亚群主要有CD4+Th1细胞、Th17细胞和Th22细胞[1]。近年来,随着对银屑病免疫学机制和易感基因研究的不断深入,根据作用机制的不同,越来越多的靶向生物制剂被研发出来用于治疗银屑病,为银屑病的系统治疗开创新纪元。     

Th22细胞与银屑病

Th22细胞是最近发现的CD4+T细胞功能亚群,表达CCR6、CCR4和CCR10,产生IL-22和IL-13,但不产生IFN-γ、IL-4和IL-17,是独立于Th1、Th2和Th17外的细胞亚群.Th22细胞在许多慢性炎症性疾病,如银屑病的发病中发挥重要作用.本文主要介绍Th22细胞和IL-22以及它们在银屑病发病中的作用及应用前景.     

Th22及其细胞因子与银屑病表达HB-EGF的关系

银屑病是皮肤科常见病、多发病,病因不清。目前认为,银屑病的发病机制主要是由T细胞介导的以角质形成细胞(KC)为靶点的免疫应答反应。辅助性T细胞22(Th22)是一种近几年新发现的T细胞亚群,其功能主要通过白细胞介素22(IL-22)来实现的。目前,对Th22细胞的研究尚处于起始阶段,对其在银屑病中的作用了解尚少。肝素结合表皮生长因子样生长因子(HB-EGF)在银屑病表皮KC异常增殖和其转归中发挥重要作用。现对Th22细胞及其细胞因子与银屑病表皮表达HB-EGF的关系进行综述。     

银屑病发病机制中免疫学研究进展

银屑病的发病机制与免疫关系密切,近几年研究倾向于银屑病是Th1/Th17混合途径的免疫性疾病.银屑病的发病中除了有树突细胞、T细胞、角质形成细胞以及Tb1型的细胞因子如白介素12、白介素18等参与外,还有Th17型细胞因子,如白介素23及白介素22等的参与,Th17型免疫反应可能在银屑病发病中起到重要的作用.     

New fillers for the new man

ABSTRACT:  Two new collagen-based lidocaine-containing dermal fillers, ArteSense™/ArteFill™ (Artes Medical, San Diego, CA) and Evolence® (Colbar LifeScience Ltd., Herzliya, Israel), have proved to be of particular interest to men, many of whom seek a long-lasting or permanent correction. ArteFill™ has been available in the United States since 2006, and it is expected that Evolence® will reach the American market in 2008. The properties of the two products will be described, and experience based on the administration of many hundreds of syringes of both products by a Canadian dermatologist will be detailed here, with tips and precautions to optimize patient outcomes.     

Outcomes and adverse effects of ablative vs nonablative lasers for skin resurfacing: A systematic review of 1093 patients

It is generally believed that ablative laser therapies result in prolonged healing and greater adverse events when compared with nonablative lasers for skin resurfacing. To evaluate the efficacy of ablative laser use for skin resurfacing and adverse events as a consequence of treatment in comparison to other modalities, a PRISMA‐compliant systematic review (Systematic Review Registration Number: 204016) of twelve electronic databases was conducted for the terms “ablative laser” and “skin resurfacing” from March 2002 until July 2020. Studies included meta‐analyses, randomized control trials, cohort studies, and case reports to facilitate evaluation of the data. All articles were evaluated for bias. The search strategy produced 34 studies. Of 1093 patients included in the studies of interest, adverse events were reported in a total of 106 patients (9.7%). Higher rates of adverse events were described in nonablative therapies (12.2% ± 2.19%, 31 events) when compared with ablative therapy (8.28% ± 2.46%, 81 events). 147 patients (13.4%) reported no side effects, 68 (6.22%) reported expected, transient self‐resolving events, and five (0.046%) presented with hypertrophic scarring. Excluding transient events, ablative lasers had fewer complications overall when compared with nonablative lasers (2.56% ± 2.19% vs 7.48% ± 3.29%). This systematic review suggests ablative laser use for skin resurfacing is a safe and effective modality to treat a range of pathologies from photodamage and acne scars to hidradenitis suppurativa and posttraumatic scarring from basal cell carcinoma excision. Further studies are needed, but these results suggest that ablative lasers are a superior, safe, and effective modality to treat damaged skin.     

Genetic alterations in RAS‐regulated pathway in acral lentiginous melanoma

Studies integrating clinicopathological and genetic features have revealed distinct patterns of genomic aberrations in Melanoma. Distributions of BRAF or NRAS mutations and gains of several oncogenes differ among melanoma subgroups, while 9p21 deletions are found in all melanoma subtypes. In the study, status of genes involved in cell cycle progression and apoptosis was evaluated in a panel of 17 frozen primary acral melanomas. NRAS mutations were found in 17% of the tumors. In contrast, BRAF mutations were not found. Gains of AURKA gene (20q13.3) were detected in 37.5% of samples, gains of CCND1 gene (11q13) or TERT gene (5p15.33) in 31.2% and gains of NRAS gene (1p13.2) in 25%. Alterations in 9p21 were identified in 69% of tumors. Gains of 11q13 and 20q13 were mutually exclusive, and 1p13.2 gain was associated with 5p15.33. Our findings showed that alterations in RAS‐related pathways are present in 87.5% of acral lentiginous melanomas.     

Self‐resolving superficial primary cutaneous mucormycosis in a 7‐week‐old infant

A 7‐week‐old girl, born at 30 weeks' gestational age, presented to clinic for evaluation of a crop of vesicular lesions that were noted after removal of a bandage that had been in place for 4 days. A punch biopsy of the lesion revealed fungal elements that were later identified as Rhizopus spp. The lesion began to self‐resolve, and no further treatment was needed, with full resolution of the lesion by 1 month after presentation. Clinicians should be aware of the variable presentations of mucormycosis and consider fungal infection in the differential diagnosis when evaluating vulnerable patients with skin eruptions.     

Pathogenic role of IL-17 in psoriasis and psoriatic arthritis

Psoriasis is a chronic inflammatory skin disorder resulting from a complex network of cytokines and chemokines produced by various immune cell types and tissue cells. Emerging evidence suggests a central role of IL-17 and IL-23/T17 axis in the pathogenesis of psoriasis, giving a rationale for using IL-17-blocking agents as therapeutics.Three agents targeting IL-17 signaling are being studied in Phase III clinical trials: secukinumab and ixekizumab (IL-17 neutralizing agents), and brodalumab (IL-17 receptor antagonist). Preliminary results are highly promising for all anti-IL17 agents, creating fair expectations on this class of agents as the new effective therapeutic approach for the treatment of psoriasis.