Arginine and immunity
Arginine and immunity
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DOI：
10.1093/jn/137.6.1681s
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发表时间：
2007-06-01
影响因子：
4.2
通讯作者：
Ochoa, Juan B.
中科院分区：
文献类型：
--
作者：
Popovic, Petar J.;Zeh, Herbert J., III;Ochoa, Juan B.
多年来，膳食精氨酸补充剂（通常与其他物质结合使用）已被用作增强免疫系统的机制。然而，关于膳食精氨酸的益处和适应症存在相当大的争议，部分原因是人们对这种氨基酸在维持免疫功能中所起的作用了解甚少。新兴知识有望消除这一争议并允许精氨酸的合理使用。在骨髓细胞中，精氨酸主要通过诱导型一氧化氮 (NO) 合酶 (iNOS) 或精氨酸酶 1（分别受 T 辅助细胞 1 或 2 细胞因子刺激的酶）代谢。因此，iNOS 或精氨酸酶（或两者）的激活反映了特定疾病过程中炎症反应的类型。骨髓抑制细胞（表达精氨酸酶的 MSC 在创伤（小鼠和人类）、腹腔内脓毒症、某些感染，尤其是癌症中都有描述。表达精氨酸酶的骨髓细胞已被证明在癌症患者体内积聚。在创伤或手术后，在单核细胞中也检测到精氨酸酶 1 表达。MSC 有效消耗精氨酸并产生鸟氨酸。通过精氨酸消耗，MSC 可以控制 NO 产生并调节其他细胞。精氨酸依赖性生物过程在创伤和癌症中已被证实，这表明 MSC 可能会产生全身效应并导致精氨酸缺乏状态，同时，T 淋巴细胞依赖于精氨酸进行增殖、zeta 链肽和 T 细胞受体复合物的表达以及记忆的发育。 zeta 链，在癌症和创伤后观察到。
For many years, dietary arginine supplementation, often combined with other substances, has been used as a mechanism to boost the immune system. Considerable controversy, however, exists as to the benefits and indications of dietary arginine due in part to a poor understanding of the role played by this amino acid in maintaining immune function. Emerging knowledge promises to clear this controversy and allow for arginine's sate use. In myeloid cells, arginine is mainly metabolized either by inducible nitric oxide (NO) synthases (iNOS) or by arginase 1, enzymes that are stimulated by T helper 1 or 2 cytokines, respectively. Thus, activation of iNOS or arginase (or both) reflects the type of inflammatory response in a specific disease process. Myeloid suppressor cells (MSC expressing arginase have been described in trauma (in both mice and humans), intra-abdominal sepsis, certain infections, and prominently, cancer. Myeloid cells expressing arginase have been shown to accumulate in patients with cancer. Arginase 1 expression is also detected in mononuclear cells after trauma or surgery. MSC efficiently deplete arginine and generate ornithine. Through arginine depletion, MSC may control NO production and regulate other arginine-dependent biological processes. Low circulating arginine has been documented in trauma and cancer, suggesting that MSC may exert a systemic effect and cause a state of arginine deficiency. Simultaneously, T lymphocytes depend on arginine for proliferation, zeta-chain peptide and T-cell receptor complex expression, and the development of memory. T-cells cocultured with MSC exhibit the molecular and functional effects associated with arginine deficiency. Not surprisingly, T-cell abnormalities, including decreased proliferation and loss of the zeta-chain, are observed in cancer and after trauma.