Contribution of Defective PS Recognition and Efferocytosis to Chronic Inflammation and Autoimmunity.
Contribution of Defective PS Recognition and Efferocytosis to Chronic Inflammation and Autoimmunity.
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DOI：
10.3389/fimmu.2014.00566
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发表时间：
2014
影响因子：
7.3
通讯作者：
Birge RB
中科院分区：
文献类型：
--
作者：
Kimani SG;Geng K;Kasikara C;Kumar S;Sriram G;Wu Y;Birge RB
凋亡细胞的快速和有效清除导致自身抗原的消除，并提供强抗炎和免疫抑制信号以防止自身免疫。尽管专职和非专职吞噬细胞利用广泛的表面受体来识别凋亡细胞，但吞噬细胞上的PS受体对凋亡细胞上的磷脂酰丝氨酸（PS）的识别是后生动物中细胞吞噬作用的标志性信号。PS依赖性红细胞增多症与抗炎因子如IL-10和TGF-β的产生相关，这些抗炎因子的部分功能是维持对自身抗原的耐受性。相反，当凋亡细胞不能被识别和处理降解时，自身抗原持续存在，例如自身核酸，其可以触发免疫激活，导致自身抗体产生和自身免疫。尽管遗传小鼠模型清楚地表明PS受体的缺失可导致年龄依赖性自身免疫疾病，使人联想到系统性红斑狼疮（SLE），但PS与慢性炎症和人类自身免疫中的清除缺陷之间的联系尚未得到很好的描述。从这个角度来看，我们审查了新出现的问题，在该领域的发展，可能是相关的SLE和人类自身免疫。
The rapid and efficient clearance of apoptotic cells results in the elimination of auto-antigens and provides a strong anti-inflammatory and immunosuppressive signal to prevent autoimmunity. While professional and non-professional phagocytes utilize a wide array of surface receptors to recognize apoptotic cells, the recognition of phosphatidylserine (PS) on apoptotic cells by PS receptors on phagocytes is the emblematic signal for efferocytosis in metazoans. PS-dependent efferocytosis is associated with the production of anti-inflammatory factors such as IL-10 and TGF-β that function, in part, to maintain tolerance to auto-antigens. In contrast, when apoptotic cells fail to be recognized and processed for degradation, auto-antigens persist, such as self-nucleic acids, which can trigger immune activation leading to autoantibody production and autoimmunity. Despite the fact that genetic mouse models clearly demonstrate that loss of PS receptors can lead to age-dependent auto-immune diseases reminiscent of systemic lupus erythematosus (SLE), the link between PS and defective clearance in chronic inflammation and human autoimmunity is not well delineated. In this perspective, we review emerging questions developing in the field that may be of relevance to SLE and human autoimmunity.
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影响因子：
13.6
作者：
Frasch SC;Bratton DL
通讯作者：
Bratton DL
影响因子：
4.4
作者：
Callahan, MK;Popernack, PM;Henderson, AJ
通讯作者：
Henderson, AJ
影响因子：
64.8
作者：
Fadok, VA;Bratton, DL;Henson, PM
通讯作者：
Henson, PM
DOI：
10.1073/pnas.1222419110
发表时间：
2013-04-09
影响因子：
11.1
作者：
Clark, Stephen R.;Thomas, Christopher P.;O'Donnell, Valerie B.
通讯作者：
O'Donnell, Valerie B.
影响因子：
--
作者：
DAVIES, EJ;SNOWDEN, N;OLLIER, WER
通讯作者：
OLLIER, WER