先前的研究发现情绪障碍与高炎症和较大的脉络丛（ChP）体积有关。炎症、ChP和二型双相抑郁（BDII-D）的临床症状之间的联系尚不清楚。基于神经解剖表型的数据驱动聚类可以帮助阐明BDII-D的神经生物学关联。本研究对150例BDII-D患者进行了炎症细胞因子、临床症状和神经解剖特征的评估。使用FreeSurfer提取了68个皮层表面积（SA）和19个皮层下结构体积。使用3D Slicer手动分割了脉络丛体积。使用正则化规范典型相关分析法识别了皮层SA和皮层下结构体积（排除ChP）之间显著相关的成分，然后使用K均值聚类定义了BDII-D的衍生大脑亚群。轻度炎症由白细胞介素（IL）-6、IL-1β和肿瘤坏死因子（TNF）-α的标准化Z值平均计算而得，以创建综合Z值分数。随后进行了部分Pearson相关分析，以探索炎症、临床症状和ChP体积之间的关联。亚群I与亚群II相比，表现出较小的皮层下结构体积和皮层SA，较高的炎症以及较大的ChP体积。ChP体积的增加与较高的轻度炎症（平均r = 0.289，q = 0.003）、CRP（平均r = 0.249，q = 0.007）、IL-6（左侧r = 0.200，q = 0.03）和TNF-α（右侧r = 0.226，q = 0.01）呈显著相关，而更高的IL-1β与BDII-D的严重抑郁症状显着相关（r = 0.218，q = 0.045）。基于神经解剖学的BDII-D亚群在炎症水平和ChP体积上有所不同。这些发现表明外周炎症的上升和较大的ChP在BDII-D中起着重要作用。本文受版权保护。版权所有。

Elevated inflammation and larger choroid plexus (ChP) volume has been previously identified in mood disorders. Connections between inflammation, ChP, and clinical symptoms in bipolar II depression (BDII-D) are unclear. Data-driven clustering based on neuroanatomical phenotypes may help to elucidate neurobiological associations in BDII-D.Inflammatory cytokines, clinical symptoms, and neuroanatomical features were assessed in 150 BDII-D patients. Sixty-eight cortical surface area (SA) and 19 subcortical volumes were extracted using FreeSurfer. The ChP volume was segmented manually using 3D Slicer. Regularized canonical correlation analysis was used to identify significantly correlated components between cortical SA and subcortical volumes (excluding the ChP), followed by k-means clustering to define brain-derived subgroups of BDII-D. Low-grade inflammation was derived by averaging the standardized z scores of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α), which were computed to create a composite z-value score. Partial Pearson correlations followed by multiple comparison correction was conducted to explore associations between inflammation, clinical symptoms, and ChP volume.Subgroup I demonstrated smaller subcortical volume and cortical SA, higher inflammation, and larger ChP volume compared with subgroup II. Greater ChP volume was associated with a higher low-grade inflammation (mean r = 0.289, q = 0.003), CRP (mean r = 0.249, q = 0.007), IL-6 (left r = 0.200, q = 0.03), and TNF-α (right r = 0.226, q = 0.01), while greater IL-1β was significantly associated with severe depressive symptoms in BDII-D (r = 0.218, q = 0.045).Neuroanatomically-derived subgroups of BDII-D differed in their inflammation levels and ChP volume. These findings suggest an important role of elevated peripheral inflammation and larger ChP in BDII-D. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.