Sepsis induces apoptosis and profound depletion of splenic interdigitating and follicular dendritic cells
Sepsis induces apoptosis and profound depletion of splenic interdigitating and follicular dendritic cells
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DOI：
10.4049/jimmunol.171.2.909
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发表时间：
2003-07-15
影响因子：
4.4
通讯作者：
Hotchkiss, RS
中科院分区：
文献类型：
--
作者：
Tinsley, KW;Grayson, MH;Hotchkiss, RS
树突状细胞是一组表型多样的APC，具有独特的能力来调节B和T细胞的活性和存活。虽然树突状细胞的正常功能对于宿主控制入侵病原体是必不可少的，但很少有研究检查脓毒症对树突状细胞的影响。本研究的目的是使用临床相关的动物模型来确定脓毒症对脾交错树突状细胞（IDC）和滤泡树突状细胞（FDC）的影响。免疫组化染色显示，脓毒症诱导FDCs的初始显着扩张，在发病后36小时达到峰值。FDC扩增以填充整个淋巴区，否则由B细胞占据。在脓毒症后36和48小时之间，存在显著的半胱天冬酶3介导的凋亡诱导的FDC耗尽，使得仅保留少量细胞。与FDCs的初始增加相反，在脓毒症发作后12小时，IDC数量下降至接近对照组的50%。IDC的死亡是由caspase 3介导的凋亡引起的。这种严重的细胞凋亡诱导的FDC和IDC的损失可能显著损害B和T细胞功能并损害宿主在脓毒症中存活的能力。
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 similar to50% 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.