与无巨细胞动脉炎 (GCA) 患者的正常 TAB 相比，鉴定具有不同炎症组织学模式：透壁炎症 (TMI) 和局限于外膜的炎症 (ILA) 的颞动脉活检 (TAB) 中的差异表达基因使用 NanoString nCounter PanCancer 免疫分析面板对来自 42 名 TMI 的 GCA 患者、7 名 ILA 的 GCA 患者和 7 名非 GCA 对照的福尔马林固定石蜡包埋的 TAB 上的 770 个免疫相关基因的表达进行分析。样本的无监督聚类揭示了两个不同的组：一组为正常 TAB 和带有 ILA 的 TAB，另一组为 41/42 带有 TMI 的 TAB。与正常 TAB 相比，带有 TMI 的 TAB 显示 31 个下调基因和 256 个上调基因；与 ILA 的 TAB 相比，他们显示出 26 个下调基因和 187 个上调基因（变化 >2.0 倍，调整后的 p 值 <0.05）。具有 ILA 的 TAB 中的基因表达与正常 TAB 相似，尽管 38 个基因表现出 >2.0 倍的变化，但这些变化在 Benjamini-Yekutieli 校正后失去了统计显着性。编码 TNF 超家族成员、免疫检查点、趋化因子和趋化因子受体、Toll 样受体、补体分子、IgG 抗体的 Fc 受体、信号淋巴细胞激活分子、JAK3、STAT1 和 STAT4 的基因在 TMI 中上调。具有 TMI 的 TAB 具有独特的转录组与正常 TAB 和 ILA TAB 相比。 ILA 中可能失调的少数基因在 TMI 中也失调。基因分析可以加深对 GCA 发病机制的了解。© 作者（或其雇主）2024。根据 CC BY-NC 允许重复使用。禁止商业再利用。请参阅权利和权限。英国医学杂志出版。

To identify differentially expressed genes in temporal artery biopsies (TABs) from patients with giant cell arteritis (GCA) with different histological patterns of inflammation: transmural inflammation (TMI) and inflammation limited to adventitia (ILA), compared with normal TABs from patients without GCA.Expression of 770 immune-related genes was profiled with the NanoString nCounter PanCancer Immune Profiling Panel on formalin-fixed paraffin-embedded TABs from 42 GCA patients with TMI, 7 GCA patients with ILA and 7 non-GCA controls.Unsupervised clustering of the samples revealed two distinct groups: normal TABs and TABs with ILA in one group, 41/42 TABs with TMI in the other one. TABs with TMI showed 31 downregulated and 256 upregulated genes compared with normal TABs; they displayed 26 downregulated and 187 upregulated genes compared with TABs with ILA (>2.0 fold changes and adjusted p values <0.05). Gene expression in TABs with ILA resembled normal TABs although 38 genes exhibited >2.0 fold changes, but these changes lost statistical significance after Benjamini-Yekutieli correction. Genes encoding TNF superfamily members, immune checkpoints, chemokine and chemokine receptors, toll-like receptors, complement molecules, Fc receptors for IgG antibodies, signalling lymphocytic activation molecules, JAK3, STAT1 and STAT4 resulted upregulated in TMI.TABs with TMI had a distinct transcriptome compared with normal TABs and TABs with ILA. The few genes potentially deregulated in ILA were also deregulated in TMI. Gene profiling allowed to deepen the knowledge of GCA pathogenesis.© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.