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脓毒症可诱导脾脏交错突细胞和滤泡树突状细胞发生凋亡并使其大量耗竭。

Sepsis induces apoptosis and profound depletion of splenic interdigitating and follicular dendritic cells.

作者信息

Tinsley Kevin W, Grayson Mitchell H, Swanson Paul E, Drewry Anne M, Chang Katherine C, Karl Irene E, Hotchkiss Richard S

机构信息

Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA.

出版信息

J Immunol. 2003 Jul 15;171(2):909-14. doi: 10.4049/jimmunol.171.2.909.

Abstract

Dendritic cells are a phenotypically diverse group of APC that have unique capabilities to regulate the activity and survival of B and T cells. Although proper function of dendritic cells is essential to host control of invading pathogens, few studies have examined the impact of sepsis on dendritic cells. The purpose of this study was to determine the effect of sepsis on splenic interdigitating dendritic cells (IDCs) and follicular dendritic cells (FDCs) using a clinically relevant animal model. Immunohistochemical staining for FDCs showed that sepsis induced an initial marked expansion in FDCs that peaked at 36 h after onset. The FDCs expanded to fill the entire lymphoid zone otherwise occupied by B cells. Between 36 and 48 h after sepsis, there was a profound caspase 3 mediated apoptosis induced depletion of FDCs such that only a small contingent of cells remained. In contrast to the initial increase in FDCs, IDC numbers were decreased to approximately 50% of control by 12 h after onset of sepsis. IDC death occurred by caspase 3-mediated apoptosis. Such profound apoptosis induced loss of FDCs and IDCs may significantly compromise B and T cell function and impair the ability of the host to survive sepsis.

摘要

树突状细胞是一群表型多样的抗原呈递细胞,具有调节B细胞和T细胞活性及存活的独特能力。尽管树突状细胞的正常功能对于宿主控制入侵病原体至关重要,但很少有研究探讨脓毒症对树突状细胞的影响。本研究的目的是使用一个临床相关的动物模型来确定脓毒症对脾脏交错突细胞(IDCs)和滤泡树突状细胞(FDCs)的影响。对FDCs的免疫组织化学染色显示,脓毒症诱导FDCs最初显著扩增,在发病后36小时达到峰值。FDCs扩增至填满原本由B细胞占据的整个淋巴区域。在脓毒症发生后36至48小时之间,出现了由半胱天冬酶3介导的深刻凋亡,导致FDCs大量耗竭,以至于仅剩下一小部分细胞。与FDCs最初的增加相反,脓毒症发病后12小时,IDC数量降至对照组的约50%。IDC死亡是由半胱天冬酶3介导的凋亡引起的。FDCs和IDCs如此深刻的凋亡诱导损失可能会显著损害B细胞和T细胞功能,并削弱宿主在脓毒症中存活的能力。

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