Eosinophils: changing perspectives in health and disease.
Eosinophils: changing perspectives in health and disease.
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DOI：
10.1038/nri3341
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发表时间：
2013-01
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嗜酸性粒细胞传统上被视为终末分化的细胞毒性效应细胞。近期研究对嗜酸性粒细胞的效应功能有了更深入的理解，对其在包括哮喘和呼吸道过敏、嗜酸性粒细胞性胃肠疾病、高嗜酸性粒细胞综合征以及寄生虫感染等多种疾病发病机制中的作用也有了更细致的认识。
嗜酸性粒细胞是粒细胞，在骨髓中由多能祖细胞响应细胞因子（如白细胞介素 - 5（IL - 5）、IL - 3和粒细胞 - 巨噬细胞集落刺激因子（GM - CSF））而发育。成熟的嗜酸性粒细胞释放到外周血中，并响应IL - 5和嗜酸粒细胞趋化因子家族趋化因子之间的协同信号进入组织。
外周血和组织中的嗜酸性粒细胞可通过其双叶核、储存细胞因子、阳离子蛋白和酶的大的特异性颗粒以及IL - 5受体和CC - 趋化因子受体3（CCR3）的表达来独特识别。此外，唾液酸结合免疫球蛋白样凝集素8（SIGLEC - 8）受体和SIGLEC - F受体分别由人和小鼠的嗜酸性粒细胞表达。
IL - 5在嗜酸性粒细胞的发育、激活和存活的各个方面都起着核心且深远的作用。IL - 5由辅助性T细胞2（TH2）产生，并且最近人们也认识到上皮来源的固有细胞因子胸腺基质淋巴细胞生成素（TSLP）、IL - 25和IL - 33通过诱导IL - 5促进嗜酸性粒细胞增多的作用。
尽管嗜酸性粒细胞的反应受T细胞产生的细胞因子影响，但嗜酸性粒细胞反过来也调节B细胞和T细胞的功能。嗜酸性粒细胞还与一系列固有免疫细胞（如肥大细胞、树突状细胞、巨噬细胞和中性粒细胞）相互作用。嗜酸性粒细胞通过调节趋化因子和细胞因子（包括CC - 趋化因子配体17（CCL17）、CCL22、增殖诱导配体（APRIL）和IL - 6）的产生以及通过抗原呈递在固有免疫和适应性免疫之间架起桥梁。
针对嗜酸性粒细胞的成功和不成功的尝试都对其在疾病发病机制中的作用产生了显著的见解。许多与嗜酸性粒细胞相关的炎症疾病在本质上已被证明是异质性的。因此，成功的治疗策略将取决于疾病活动与失调的嗜酸性粒细胞功能之间的相关性，以及对调节嗜酸性粒细胞在受影响组织中积聚的关键分子的识别。
本文的网络版（doi:10.1038/nri3341）包含补充材料，授权用户可获取。
这篇综述描述了嗜酸性粒细胞独特的生物学特性。作者解释了嗜酸性粒细胞如何与其他白细胞群体相互作用，以在感染后促进保护性免疫。他们还讨论了嗜酸性粒细胞在过敏类疾病（如哮喘和高嗜酸性粒细胞综合征）中的病理作用。
本文的网络版（doi:10.1038/nri3341）包含补充材料，授权用户可获取。
嗜酸性粒细胞传统上被视为终末分化的细胞毒性效应细胞。近期研究极大地改变了这种对嗜酸性粒细胞及其功能的简单看法。对控制嗜酸性粒细胞发育、转运和脱颗粒的分子途径的新见解提高了我们对这些细胞免疫调节功能及其在促进内环境稳定中的作用的理解。同样，近期的研究进展使我们对嗜酸性粒细胞如何在包括哮喘和原发性高嗜酸性粒细胞综合征等不同疾病的发病机制中起作用有了更复杂的认识，也使我们对这些细胞在寄生虫感染期间的活动有了更全面的了解。
本文的网络版（doi:10.1038/nri3341）包含补充材料，授权用户可获取。
Eosinophils have been traditionally perceived as terminally differentiated cytotoxic effector cells. Recent studies have provided a more sophisticated understanding of eosinophil effector functions and a more nuanced view of their contributions to the pathogenesis of various diseases, including asthma and respiratory allergies, eosinophilic gastrointestinal diseases, hypereosinophilic syndromes and parasitic infection. Eosinophils are granulocytes that develop in the bone marrow from pluripotent progenitors in response to cytokines, such as interleukin-5 (IL-5), IL-3 and granulocyte–macrophage colony-stimulating factor (GM-CSF). Mature eosinophils are released into the peripheral blood and enter tissues in response to cooperative signalling between IL-5 and eotaxin family chemokines. Eosinophils in peripheral blood and tissues are uniquely identified by their bilobed nuclei, their large specific granules that store cytokines, cationic proteins and enzymes, and their expression of the IL-5 receptor and CC-chemokine receptor 3 (CCR3). In addition, the receptors sialic acid-binding immunoglobulin-like lectin 8 (SIGLEC-8) and SIGLEC-F are expressed by human and mouse eosinophils, respectively. IL-5 has a central and profound role in all aspects of eosinophil development, activation and survival. IL-5 is produced by T helper 2 (TH2) cells, and more recently the contributions of the epithelium-derived innate cytokines thymic stromal lymphopoietin (TSLP), IL-25 and IL-33 in promoting eosinophilia via the induction of IL-5 have also been recognized. Although eosinophil responses are influenced by cytokines produced by T cells, eosinophils in turn modulate the functions of B and T cells. Eosinophils also communicate with a range of innate immune cells (such as mast cells, dendritic cells, macrophages and neutrophils). Eosinophils serve to bridge innate and adaptive immunity by regulating the production of chemoattractants and cytokines (including CC-chemokine ligand 17 (CCL17), CCL22, a proliferation-inducing ligand (APRIL) and IL-6) and via antigen presentation. Both successful and unsuccessful attempts to target eosinophils have yielded remarkable insights into their contribution to disease pathogenesis. Many eosinophil-associated inflammatory conditions have been shown to be heterogeneous in nature. As such, successful therapeutic strategies will depend on the correlation of disease activity with dysregulated eosinophil function as well as the identification of the crucial molecules that regulate eosinophil accumulation in the affected tissues. The online version of this article (doi:10.1038/nri3341) contains supplementary material, which is available to authorized users. This Review describes the unique biology of the eosinophil. The authors explain how eosinophils interact with other leukocyte populations to promote protective immunity following infection. They also discuss the pathological roles of eosinophils in allergic-type diseases, such as asthma and the hypereosinophilic syndromes. The online version of this article (doi:10.1038/nri3341) contains supplementary material, which is available to authorized users. Eosinophils have been traditionally perceived as terminally differentiated cytotoxic effector cells. Recent studies have profoundly altered this simplistic view of eosinophils and their function. New insights into the molecular pathways that control the development, trafficking and degranulation of eosinophils have improved our understanding of the immunomodulatory functions of these cells and their roles in promoting homeostasis. Likewise, recent developments have generated a more sophisticated view of how eosinophils contribute to the pathogenesis of different diseases, including asthma and primary hypereosinophilic syndromes, and have also provided us with a more complete appreciation of the activities of these cells during parasitic infection. The online version of this article (doi:10.1038/nri3341) contains supplementary material, which is available to authorized users.
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影响因子：
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