Immunologic Features in Coronavirus Disease 2019: Functional Exhaustion of T Cells and Cytokine Storm
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LETTER TO EDITOR
Immunologic Features in Coronavirus Disease 2019: Functional Exhaustion of T Cells and Cytokine Storm Shima Mahmoudi 1 & Mitra Rezaei 2 & Nahal Mansouri 3,4 & Majid Marjani 5
&
Davood Mansouri 4,5
Received: 23 April 2020 / Accepted: 3 July 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
To the Editor: Since the emergence of Coronavirus Disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in December 2019, the number of severe forms of SARS-CoV-2 infection is rising quickly and causes a large number of deaths throughout the world. By June 16, 2020, the total number of laboratoryconfirmed cases of COVID-19 surpassed 7,941,791, with 434,796 reported deaths worldwide [1]. Actually, mortality may be higher due to deaths from unrecognized COVID-19 and deaths resulting from diminished routine diagnosis and treatment of other conditions [2]. SARS-CoV-2 infection is divided into three main categories including asymptomatic, non-severe symptomatic, and severe respiratory and systemic presentations [3]. Older age, high level of D-dimer concentrations, and the neutrophil to lymphocyte ratio are reported as independent risk factor predictors for the in-hospital mortality in hospitalized COVID-19 patients [4]. The immune response plays an important role in
* Majid Marjani [email protected] 1
Pediatric Infectious Disease Research Center, Tehran University of Medical Sciences, Tehran, Iran
2
Virology Research Center, National Research Institute of Tuberculosis and Lung diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran
3
Division of Pulmonary Medicine, Department of Medicine, Lausanne University Hospital (CHUV), University of Lausanne (UNIL), Lausanne, Switzerland
4
Department of Clinical Immunology and Infectious Diseases, National Research Institute of Tuberculosis and Lung Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran
5
Clinical Tuberculosis and Epidemiology Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran
the control and resolution of COVID-19. However, little is known about lymphocyte subsets and the immune response of patients with COVID-19 [5]. Following binding of the S proteins of SARS-CoV-2 by angiotensin-converting enzyme 2 (ACE2) to the host cells, fusing to the membrane and release of the viral RNA, pathogen-associated molecular patterns are detected by the pattern recognition receptors. Consequently, the complex dynamic signaling, as well as downstream cascade molecules, contribute to activation of the transcription factors consisting of nuclear factor-κB (NF-κB) and interferon regulatory factor 3 (IRF3), resulting in the production of type I interferons (IFN-α/β) and a series of pro-inflammatory cytokines [6]. SARS-CoV-2 infection causes innate and adaptive immune responses resulting in diverse setup immune mediators contributing to the disease severity an
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