Brief Report: Altered Innate Lymphoid Cell Subsets in Human Lymph Node Biopsy Specimens Obtained During the At-Risk and Earliest Phases of Rheumatoid Arthritis.
Brief Report: Altered Innate Lymphoid Cell Subsets in Human Lymph Node Biopsy Specimens Obtained During the At-Risk and Earliest Phases of Rheumatoid Arthritis.
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DOI：
10.1002/art.39811
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发表时间：
2017-01
期刊：
影响因子：
--
通讯作者：
van Baarsen LG
中科院分区：
文献类型：
--
作者：
Rodríguez-Carrio J;Hähnlein JS;Ramwadhdoebe TH;Semmelink JF;Choi IY;van Lienden KP;Maas M;Gerlag DM;Tak PP;Geijtenbeek TB;van Baarsen LG
先天性淋巴样细胞（ILC）是新兴的免疫介质，炎症性ILC群体的蓄积可发生在炎症介导的疾病中。由于早期淋巴结（LN）活化已被证明在类风湿关节炎（RA），我们的目的是调查的频率和分布在LN活检标本在RA的最早阶段。12例早期RA患者，12例IgM类风湿因子和/或抗瓜氨酸蛋白抗体无关节炎的个体（RA风险组）和7例健康对照接受超声引导腹股沟LN活检。采用流式细胞仪检测LN内皮细胞和成纤维细胞的血管细胞粘附分子（VCAM）和细胞间粘附分子（ICAM）的表达。虽然未发现总ILC（Lin− CD 45 +/lowCD 127+）的频率存在差异，但ILC亚群的分布在各组之间存在差异。与对照组相比，RA患者显示淋巴组织诱导（LTi）细胞（c-Kit + NKp 44 − ILC）数量减少，ILC 1（c-Kit − NKp 44 − ILC）和ILC 3（c-Kit + NKp 44 + ILC）数量增加（分别为P < 0.001，P < 0.050和P < 0.050）。RA高危人群ILC 1基因频率高于对照组（P < 0.01）。LTi细胞抑制内皮细胞和成纤维细胞粘附分子的表达。我们的研究结果表明，在RA的风险和早期阶段，LN中的ILC分布从稳态分布向更具炎症性的分布变化，从而提供了ILC在RA发病机制中的作用的证据。
Innate lymphoid cells (ILCs) are emerging mediators of immunity, and accumulation of inflammatory ILC populations can occur in inflammatory‐mediated conditions. Since early lymph node (LN) activation has been shown in rheumatoid arthritis (RA), we aimed to investigate the frequency and distribution of ILCs in LN biopsy specimens obtained during the earliest phases of RA. Twelve patients with early RA, 12 individuals with IgM rheumatoid factor and/or anti–citrullinated protein antibodies without arthritis (RA risk group), and 7 healthy controls underwent ultrasound‐guided inguinal LN biopsy. ILC subsets and the expression of vascular cell adhesion molecule (VCAM) and intercellular adhesion molecule (ICAM) by LN endothelial cells and fibroblasts were analyzed by flow cytometry. Although no differences in the frequencies of total ILCs (Lin−CD45+/lowCD127+) were found, the distribution of the ILC subpopulations differed among groups. RA patients showed lower numbers of lymphoid tissue–inducer (LTi) cells (c‐Kit+NKp44− ILCs) and increased ILC1 (c‐Kit−NKp44− ILCs) and ILC3 (c‐Kit+NKp44+ ILCs) numbers compared with controls (P < 0.001, P < 0.050, and P < 0.050, respectively). Individuals at risk of RA exhibited an increased frequency of ILC1 compared with controls (P < 0.01). LTi cells paralleled the expression of adhesion molecules on endothelial cells and fibroblasts. Our findings indicate that during the at‐risk and earliest phases of RA, the ILC distribution in LN changes from a homeostatic profile toward a more inflammatory profile, thereby providing evidence of a role for ILCs in RA pathogenesis.
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影响因子：
27.4
作者：
Gerlag DM;Raza K;van Baarsen LG;Brouwer E;Buckley CD;Burmester GR;Gabay C;Catrina AI;Cope AP;Cornelis F;Dahlqvist SR;Emery P;Eyre S;Finckh A;Gay S;Hazes JM;van der Helm-van Mil A;Huizinga TW;Klareskog L;Kvien TK;Lewis C;Machold KP;Rönnelid J;van Schaardenburg D;Schett G;Smolen JS;Thomas S;Worthington J;Tak PP
通讯作者：
Tak PP
影响因子：
32.4
作者：
Powell N;Walker AW;Stolarczyk E;Canavan JB;Gökmen MR;Marks E;Jackson I;Hashim A;Curtis MA;Jenner RG;Howard JK;Parkhill J;MacDonald TT;Lord GM
通讯作者：
Lord GM
影响因子：
30.5
作者：
Bernink, Jochem H.;Peters, Charlotte P.;Spits, Hergen
通讯作者：
Spits, Hergen
影响因子：
64.8
作者：
Shiow, LR;Rosen, DB;Matloubian, M
通讯作者：
Matloubian, M
影响因子：
32.4
作者：
Fuchs A;Vermi W;Lee JS;Lonardi S;Gilfillan S;Newberry RD;Cella M;Colonna M
通讯作者：
Colonna M