Triggianese Paola, Conigliaro Paola, Chimenti Maria Sole, Biancone Livia, Monteleone Giovanni, Perricone Roberto, Monteleone Ivan
Rheumatology, Allergology and Clinical Immunology, Department of Medicina dei Sistemi, University of Rome Tor Vergata, Rome, Italy.
Gastrointestinal Unit, Department of Medicina dei Sistemi, University of Rome Tor Vergata, Rome, Italy.
Clin Exp Rheumatol. 2016 Nov-Dec;34(6):1085-1093. Epub 2016 Oct 21.
Both the innate and the adaptive immune responses contribute to the onset of chronic inflammation in spondyloarthritis (SpA). The association between SpA and inflammatory bowel disease (IBD, enteropathic SpA-ESpA) has been largely established and suggests a shared pathophysiology. There is evidence that innate lymphoid cells (ILC) are involved in the pathogenesis of both SpA and IBD while no evidence has been reported to date on ESpA. We aimed to analyse for the first time the frequency and cytokine expression of ILC in peripheral blood from ESpA patients compared with both IBD and healthy subjects. Correlations between immunophenotyping and disease activity were also explored.
ESpA patients (n=20) were prospectively enrolled. Healthy controls (HC, n=10) and IBD patients (n=10) served as control groups. Peripheral blood Interferon (IFN)-γ and interleukin (IL)-17 expressing T and non-T cells as well as ILC subsets (ILC-1: IFN- γ +; ILC-3: IL-17+; natural killer-NK) were characterised by flowcytometry. Correlations between IL-17+ cells and SpA disease activity were analysed.
ESpA patients showed higher levels of ROR-γ expressing non T-cells with the respect to the controls. IL-17 producing non-T cells were higher than the HC and positively correlated with IFN-γ expressing cells levels as well as with SpA disease activity. ESpA showed higher levels of ILC-1 and ILC-3 than both IBD and HC. IFN-γ expressing NK cells were higher in ESpA than HC.
Our preliminary findings indicate that peripheral blood of ESpA patients is enriched for IL-17 expressing ILC which distinguishes the blood compartment from both IBD and HC. The increased IL-17 production by ILC indicates a novel role for ILC in ESpA.
先天性免疫反应和适应性免疫反应均参与了脊柱关节炎（SpA）慢性炎症的发生。SpA与炎症性肠病（IBD，肠病性SpA-ESpA）之间的关联已基本明确，提示二者存在共同的病理生理学机制。有证据表明，固有淋巴细胞（ILC）参与了SpA和IBD的发病机制，但迄今为止，尚无关于ESpA的相关报道。我们旨在首次分析ESpA患者外周血中ILC的频率和细胞因子表达，并与IBD患者和健康受试者进行比较。同时，还探讨了免疫表型与疾病活动度之间的相关性。
前瞻性纳入20例ESpA患者。健康对照组（HC，n = 10）和IBD患者（n = 10）作为对照组。采用流式细胞术对外周血中表达干扰素（IFN）-γ和白细胞介素（IL）-17的T细胞和非T细胞以及ILC亚群（ILC-1：IFN-γ+；ILC-3：IL-17+；自然杀伤细胞-NK）进行表征。分析IL-17+细胞与SpA疾病活动度之间的相关性。
与对照组相比，ESpA患者中表达ROR-γ的非T细胞水平更高。产生IL-17的非T细胞高于HC组，且与表达IFN-γ的细胞水平以及SpA疾病活动度呈正相关。ESpA患者的ILC-1和ILC-3水平高于IBD患者和HC组。ESpA患者中表达IFN-γ的NK细胞高于HC组。
我们的初步研究结果表明，ESpA患者外周血中富含表达IL-17的ILC，这使其血液成分与IBD患者和HC组有所区别。ILC产生IL-17的增加表明ILC在ESpA中具有新的作用。
