New sights of low dose IL‐2: Restoration of immune homeostasis for viral infection

Author:

Su Rui12ORCID,Zhang Tingting12,Wang Hui12,Yan Gaofei3,Wu Ruihe12,Zhang Xin12,Gao Chong4,Li Xiaofeng12,Wang Caihong12

Affiliation:

1. Department of Rheumatology The Second Hospital of Shanxi Medical University Taiyuan Shanxi China

2. Shanxi Key Laboratory of Immunomicroecology Taiyuan Shanxi China

3. Second department Hamony Long Stomatological Hospital Taiyuan China

4. Department of Pathology, Brigham and Women's Hospital/Children's Hospital Boston, Joint Program in Transfusion Medicine Harvard Medical School Boston Massachusetts USA

Abstract

AbstractViral infection poses a significant threat to human health. In addition to the damage caused by viral replication, the immune response it triggers often leads to more serious adverse consequences. After the occurrence of viral infection, in addition to the adverse consequences of infection, chronic infections can also lead to virus‐related autoimmune diseases and tumours. At the same time, the immune response triggered by viral infection is complex, and dysregulated immune response may lead to the occurrence of immune pathology and macrophage activation syndrome. In addition, it may cause secondary immune suppression, especially in patients with compromised immune system, which could lead to the occurrence of secondary infections by other pathogens. This can often result in more severe clinical outcomes. Therefore, regarding the treatment of viral infections, restoring the balance of the immune system is crucial in addition to specific antiviral medications. In recent years, scientists have made an interesting finding that low dose IL‐2 (ld‐IL‐2) could potentially have a crucial function in regulating the immune system and reducing the chances of infection, especially viral infection. Ld‐IL‐2 exerts immune regulatory effects in different types of viral infections by modulating CD4+T subsets, CD8+T cells, natural killer cells, and so on. Our review summarised the role of IL‐2 or IL‐2 complexes in viral infections. Ld‐IL‐2 may be an effective strategy for enhancing host antiviral immunity and preventing infection from becoming chronic; additionally, the appropriate use of it can help prevent excessive inflammatory response after infection. In the long term, it may reduce the occurrence of infection‐related autoimmune diseases and tumours by promoting the restoration of early immune homeostasis. Furthermore, we have also summarised the application of ld‐IL‐2 in the context of autoimmune diseases combined with viral infections; it may be a safe and effective strategy for restoring immune homeostasis without compromising the antiviral immune response. In conclusion, focusing on the role of ld‐IL‐2 in viral infections may provide a new perspective for regulating immune responses following viral infections and improving prognosis.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Immunology,Immunology and Allergy

Reference119 articles.

1. Sepsis‐induced immunosuppression: mechanisms, diagnosis and current treatment options;Liu D;Mil Med Res,2022

2. Imbalance between Th17 and regulatory T cells in patients with systemic lupus erythematosus combined EBV/CMV viraemia;Su R;Clin Exp Rheumatol,2020

3. Endogenous IL‐2 contributes to T cell expansion and IFN‐gamma production during lymphocytic choriomeningitis virus infection;Cousens LP;J Immunol,1995

4. Immunological and clinical effects of low‐dose interleukin‐2 across 11 autoimmune diseases in a single, open clinical trial;Rosenzwajg M;Ann Rheum Dis,2019

5. Low‐dose Interleukin‐2: biology and therapeutic prospects in rheumatoid arthritis;Wu R;Autoimmun Rev,2020

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3