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Reduced abundance of butyric acid-producing bacteria in the ileal mucosa-associated microbiota of ulcerative colitis patients.溃疡性结肠炎患者回肠黏膜相关微生物群中丁酸产生菌的丰度降低。
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Continuous germinal center invasion contributes to the diversity of the immune response.持续的生发中心入侵有助于免疫反应的多样性。
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在 HIV-1 感染中,胃肠道生发中心 B 细胞耗竭和 IgA 浆细胞减少。

Gastrointestinal germinal center B cell depletion and reduction in IgA plasma cells in HIV-1 infection.

机构信息

Division of Infectious Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

出版信息

Sci Immunol. 2024 Oct 25;9(100):eado0090. doi: 10.1126/sciimmunol.ado0090.

DOI:10.1126/sciimmunol.ado0090
PMID:39454027
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11557871/
Abstract

Gastrointestinal (GI) B cells and plasma cells (PCs) are critical to mucosal homeostasis and the host response to HIV-1 infection. Here, high-resolution mapping of human B cells and PCs sampled from the colon and ileum during both viremic and suppressed HIV-1 infection identified a reduction in germinal center (GC) B cells and follicular dendritic cells (FDCs) during HIV-1 viremia. Immunoglobulin A-positive (IgA) PCs are the major cellular output of intestinal GCs and were significantly reduced during viremic HIV-1 infection. PC-associated transcriptional perturbations, including type I interferon signaling, persisted in antiretroviral therapy (ART)-treated individuals, suggesting ongoing disruption of the intestinal immune milieu during ART. GI humoral immune perturbations were associated with changes in the intestinal microbiome composition and systemic inflammation. These findings highlight a key immune defect in the GI mucosa due to HIV-1 viremia.

摘要

胃肠道 (GI) B 细胞和浆细胞 (PCs) 对于黏膜稳态和宿主对 HIV-1 感染的反应至关重要。在这里,对病毒血症和抑制的 HIV-1 感染期间从结肠和回肠中取样的人类 B 细胞和 PCs 进行高分辨率绘图,确定在 HIV-1 病毒血症期间生发中心 (GC) B 细胞和滤泡树突状细胞 (FDC) 减少。免疫球蛋白 A 阳性 (IgA) PCs 是肠道 GCs 的主要细胞输出物,在病毒血症 HIV-1 感染期间显著减少。与 PC 相关的转录扰动,包括 I 型干扰素信号,在接受抗逆转录病毒治疗 (ART) 的个体中持续存在,这表明在 ART 期间肠道免疫环境持续受到破坏。GI 体液免疫扰动与肠道微生物组组成和全身炎症的变化有关。这些发现强调了由于 HIV-1 病毒血症导致的 GI 黏膜中的关键免疫缺陷。

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