{"title":"COVID-19 感染中的趋化因子受体","authors":"Claudia Gutierrez-Chavez, Shalom Aperrigue-Lira, Brando Ortiz-Saavedra, Irmia Paz","doi":"10.1016/bs.ircmb.2024.05.002","DOIUrl":null,"url":null,"abstract":"<p><p>Chemokine receptors play diverse roles in the immune response against pathogens by recruiting innate and adaptive immune cells to sites of infection. However, their involvement could also be detrimental, causing tissue damage and exacerbating respiratory diseases by triggering histological alterations such as fibrosis and remodeling. This chapter reviews the role of chemokine receptors in the immune defense against SARS-CoV-2 infection. In COVID-19, CXCR3 is expressed mainly in T cells, and its upregulation is related to an increase in SARS-CoV-2-specific antibodies but also to COVID-19 severity. CCR5 is a key player in T-cell recruitment, and its suppression leads to reduced inflammation and viremia levels. Conversely, CXCR6 is implicated in the aberrant migration of memory T cells within airways. On the other hand, increased CCR4+ cells in the blood and decreased CCR4+ cells in lung cells are associated with severe COVID-19. Additionally, CCR2 is associated with an increase in macrophage recruitment to lung tissues. Elevated levels of CXCR1 and CXCR2, which are predominantly expressed in neutrophils, are associated with the severity of the disease, and finally, the expression of CX3CR1 in cytotoxic T lymphocytes affects the retention of these cells in lung tissues, thereby impacting the severity of COVID-19. Despite the efforts of many clinical trials to find effective therapies for COVID-19 using chemokine receptor inhibitors, no conclusive results have been found due to the small number of patients, redundancy, and co-expression of chemokine receptors by immune cells, which explains the difficulty in finding a single therapeutic target or effective treatment.</p>","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"388 ","pages":"53-94"},"PeriodicalIF":0.0000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Chemokine receptors in COVID-19 infection.\",\"authors\":\"Claudia Gutierrez-Chavez, Shalom Aperrigue-Lira, Brando Ortiz-Saavedra, Irmia Paz\",\"doi\":\"10.1016/bs.ircmb.2024.05.002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Chemokine receptors play diverse roles in the immune response against pathogens by recruiting innate and adaptive immune cells to sites of infection. However, their involvement could also be detrimental, causing tissue damage and exacerbating respiratory diseases by triggering histological alterations such as fibrosis and remodeling. This chapter reviews the role of chemokine receptors in the immune defense against SARS-CoV-2 infection. In COVID-19, CXCR3 is expressed mainly in T cells, and its upregulation is related to an increase in SARS-CoV-2-specific antibodies but also to COVID-19 severity. CCR5 is a key player in T-cell recruitment, and its suppression leads to reduced inflammation and viremia levels. Conversely, CXCR6 is implicated in the aberrant migration of memory T cells within airways. On the other hand, increased CCR4+ cells in the blood and decreased CCR4+ cells in lung cells are associated with severe COVID-19. Additionally, CCR2 is associated with an increase in macrophage recruitment to lung tissues. Elevated levels of CXCR1 and CXCR2, which are predominantly expressed in neutrophils, are associated with the severity of the disease, and finally, the expression of CX3CR1 in cytotoxic T lymphocytes affects the retention of these cells in lung tissues, thereby impacting the severity of COVID-19. Despite the efforts of many clinical trials to find effective therapies for COVID-19 using chemokine receptor inhibitors, no conclusive results have been found due to the small number of patients, redundancy, and co-expression of chemokine receptors by immune cells, which explains the difficulty in finding a single therapeutic target or effective treatment.</p>\",\"PeriodicalId\":14422,\"journal\":{\"name\":\"International review of cell and molecular biology\",\"volume\":\"388 \",\"pages\":\"53-94\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International review of cell and molecular biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1016/bs.ircmb.2024.05.002\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/6/30 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International review of cell and molecular biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/bs.ircmb.2024.05.002","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/6/30 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 0
摘要
趋化因子受体通过招募先天性和适应性免疫细胞到感染部位,在针对病原体的免疫反应中发挥着多种作用。然而,趋化因子受体的参与也可能是有害的,它们会引发组织学改变,如纤维化和重塑,从而造成组织损伤并加重呼吸系统疾病。本章回顾了趋化因子受体在抵抗 SARS-CoV-2 感染的免疫防御中的作用。在 COVID-19 中,CXCR3 主要在 T 细胞中表达,它的上调与 SARS-CoV-2 特异性抗体的增加有关,也与 COVID-19 的严重程度有关。CXCR5 是 T 细胞招募的关键因素,抑制它可降低炎症和病毒血症水平。相反,CXCR6 与记忆 T 细胞在气道内的异常迁移有关。另一方面,血液中 CCR4+ 细胞的增加和肺细胞中 CCR4+ 细胞的减少与严重的 COVID-19 有关。此外,CCR2 与巨噬细胞招募到肺组织的增加有关。主要在中性粒细胞中表达的 CXCR1 和 CXCR2 水平升高与疾病的严重程度有关,最后,细胞毒性 T 淋巴细胞中 CX3CR1 的表达会影响这些细胞在肺组织中的滞留,从而影响 COVID-19 的严重程度。尽管许多临床试验都在努力寻找使用趋化因子受体抑制剂治疗 COVID-19 的有效疗法,但由于患者人数较少、免疫细胞中趋化因子受体的冗余和共表达,因此很难找到单一的治疗靶点或有效的治疗方法,目前还没有发现结论性的结果。
Chemokine receptors play diverse roles in the immune response against pathogens by recruiting innate and adaptive immune cells to sites of infection. However, their involvement could also be detrimental, causing tissue damage and exacerbating respiratory diseases by triggering histological alterations such as fibrosis and remodeling. This chapter reviews the role of chemokine receptors in the immune defense against SARS-CoV-2 infection. In COVID-19, CXCR3 is expressed mainly in T cells, and its upregulation is related to an increase in SARS-CoV-2-specific antibodies but also to COVID-19 severity. CCR5 is a key player in T-cell recruitment, and its suppression leads to reduced inflammation and viremia levels. Conversely, CXCR6 is implicated in the aberrant migration of memory T cells within airways. On the other hand, increased CCR4+ cells in the blood and decreased CCR4+ cells in lung cells are associated with severe COVID-19. Additionally, CCR2 is associated with an increase in macrophage recruitment to lung tissues. Elevated levels of CXCR1 and CXCR2, which are predominantly expressed in neutrophils, are associated with the severity of the disease, and finally, the expression of CX3CR1 in cytotoxic T lymphocytes affects the retention of these cells in lung tissues, thereby impacting the severity of COVID-19. Despite the efforts of many clinical trials to find effective therapies for COVID-19 using chemokine receptor inhibitors, no conclusive results have been found due to the small number of patients, redundancy, and co-expression of chemokine receptors by immune cells, which explains the difficulty in finding a single therapeutic target or effective treatment.
期刊介绍:
International Review of Cell and Molecular Biology presents current advances and comprehensive reviews in cell biology-both plant and animal. Articles address structure and control of gene expression, nucleocytoplasmic interactions, control of cell development and differentiation, and cell transformation and growth. Authored by some of the foremost scientists in the field, each volume provides up-to-date information and directions for future research.