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1.
Int J Mol Sci ; 23(1)2021 Dec 31.
Article in English | MEDLINE | ID: covidwho-1580694

ABSTRACT

Telomeres are localized at the end of chromosomes to provide genome stability; however, the telomere length tends to be shortened with each cell division inducing a progressive telomere shortening (TS). In addition to age, other factors, such as exposure to pollutants, diet, stress, and disruptions in the shelterin protein complex or genes associated with telomerase induce TS. This phenomenon favors cellular senescence and genotoxic stress, which increases the risk of the development and progression of lung diseases such as idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, SARS-CoV-2 infection, and lung cancer. In an infectious environment, immune cells that exhibit TS are associated with severe lymphopenia and death, whereas in a noninfectious context, naïve T cells that exhibit TS are related to cancer progression and enhanced inflammatory processes. In this review, we discuss how TS modifies the function of the immune system cells, making them inefficient in maintaining homeostasis in the lung. Finally, we discuss the advances in drug and gene therapy for lung diseases where TS could be used as a target for future treatments.


Subject(s)
Lung Diseases/genetics , Lung Diseases/immunology , Telomere Shortening/immunology , Animals , COVID-19/genetics , COVID-19/immunology , Cellular Senescence/genetics , Genetic Therapy/methods , Humans , Immunotherapy/methods , Lung Diseases/drug therapy
2.
Front Immunol ; 12: 710375, 2021.
Article in English | MEDLINE | ID: covidwho-1518483

ABSTRACT

The unique environment of the lungs is protected by complex immune interactions. Human lung tissue-resident memory T cells (TRM) have been shown to position at the pathogen entry points and play an essential role in fighting against viral and bacterial pathogens at the frontline through direct mechanisms and also by orchestrating the adaptive immune system through crosstalk. Recent evidence suggests that TRM cells also play a vital part in slowing down carcinogenesis and preventing the spread of solid tumors. Less beneficially, lung TRM cells can promote pathologic inflammation, causing chronic airway inflammatory changes such as asthma and fibrosis. TRM cells from infiltrating recipient T cells may also mediate allograft immunopathology, hence lung damage in patients after lung transplantations. Several therapeutic strategies targeting TRM cells have been developed. This review will summarize recent advances in understanding the establishment and maintenance of TRM cells in the lung, describe their roles in different lung diseases, and discuss how the TRM cells may guide future immunotherapies targeting infectious diseases, cancers and pathologic immune responses.


Subject(s)
Lung Diseases/immunology , Lung/immunology , /immunology , Animals , Humans , Lymphocytes, Tumor-Infiltrating/immunology , Mice , Neoadjuvant Therapy , Vaccines/immunology
3.
Front Immunol ; 12: 753940, 2021.
Article in English | MEDLINE | ID: covidwho-1463477

ABSTRACT

Lung macrophages play important roles in the maintenance of homeostasis, pathogen clearance and immune regulation. The different types of pulmonary macrophages and their roles in lung diseases have attracted attention in recent years. Alveolar macrophages (AMs), including tissue-resident alveolar macrophages (TR-AMs) and monocyte-derived alveolar macrophages (Mo-AMs), as well as interstitial macrophages (IMs) are the major macrophage populations in the lung and have unique characteristics in both steady-state conditions and disease states. The different characteristics of these three types of macrophages determine the different roles they play in the development of disease. Therefore, it is important to fully understand the similarities and differences among these three types of macrophages for the study of lung diseases. In this review, we will discuss the physiological characteristics and unique functions of these three types of macrophages in acute and chronic lung diseases. We will also discuss possible methods to target macrophages in lung diseases.


Subject(s)
COVID-19/immunology , Lung Diseases/immunology , Lung/immunology , Macrophages/immunology , SARS-CoV-2/physiology , Animals , Homeostasis , Humans , Inflammation
4.
Life Sci ; 283: 119871, 2021 Oct 15.
Article in English | MEDLINE | ID: covidwho-1336712

ABSTRACT

Non-communicable, chronic respiratory diseases (CRDs) affect millions of individuals worldwide. The course of these CRDs (asthma, chronic obstructive pulmonary disease, and cystic fibrosis) are often punctuated by microbial infections that may result in hospitalization and are associated with increased risk of morbidity and mortality, as well as reduced quality of life. Interleukin-13 (IL-13) is a key protein that regulates airway inflammation and mucus hypersecretion. There has been much interest in IL-13 from the last two decades. This cytokine is believed to play a decisive role in the exacerbation of inflammation during the course of viral infections, especially, in those with pre-existing CRDs. Here, we discuss the common viral infections in CRDs, as well as the potential role that IL-13 plays in the virus-induced disease pathogenesis of CRDs. We also discuss, in detail, the immune-modulation potential of IL-13 that could be translated to in-depth studies to develop IL-13-based therapeutic entities.


Subject(s)
Influenza, Human/immunology , Interleukin-13/immunology , Lung Diseases/immunology , Chronic Disease , Humans , Inflammation/immunology , Inflammation/pathology , Influenza, Human/pathology , Lung Diseases/pathology , Mucus/immunology
6.
Chem Biol Interact ; 345: 109568, 2021 Aug 25.
Article in English | MEDLINE | ID: covidwho-1283962

ABSTRACT

Nuclear factor-kappa B, involved in inflammation, host immune response, cell adhesion, growth signals, cell proliferation, cell differentiation, and apoptosis defense, is a dimeric transcription factor. Inflammation is a key component of many common respiratory disorders, including asthma, chronic obstructive pulmonary disease (COPD), bronchiectasis, and acute respiratory distress syndrome. Many basic transcription factors are found in NF-κB signaling, which is a member of the Rel protein family. Five members of this family c-REL, NF-κB2 (p100/p52), RelA (p65), NF-κB1 (p105/p50), RelB, and RelA (p65) produce 5 transcriptionally active molecules. Proinflammatory cytokines, T lymphocyte, and B lymphocyte cell mitogens, lipopolysaccharides, bacteria, viral proteins, viruses, double-stranded RNA, oxidative stress, physical exertion, various chemotherapeutics are the stimulus responsible for NF-κB activation. NF-κB act as a principal component for several common respiratory illnesses, such as asthma, lung cancer, pulmonary fibrosis, COPD as well as infectious diseases like pneumonia, tuberculosis, COVID-19. Inflammatory lung disease, especially COVID-19, can make NF-κB a key target for drug production.


Subject(s)
Lung Diseases/metabolism , NF-kappa B/metabolism , Animals , Humans , Inflammation/complications , Lung Diseases/complications , Lung Diseases/drug therapy , Lung Diseases/immunology
7.
Front Immunol ; 12: 656362, 2021.
Article in English | MEDLINE | ID: covidwho-1211814

ABSTRACT

Since March 2020, the outbreak of Sars-CoV-2 pandemic has changed medical practice and daily routine around the world. Huge efforts from pharmacological industries have led to the development of COVID-19 vaccines. In particular two mRNA vaccines, namely the BNT162b2 (Pfizer-BioNTech) and the mRNA-1273 (Moderna), and a viral-vectored vaccine, i.e. ChAdOx1 nCoV-19 (AstraZeneca), have recently been approved in Europe. Clinical trials on these vaccines have been published on the general population showing a high efficacy with minor adverse events. However, specific data about the efficacy and safety of these vaccines in patients with immune-mediated inflammatory diseases (IMIDs) are still lacking. Moreover, the limited availability of these vaccines requires prioritizing some vulnerable categories of patients compared to others. In this position paper, we propose the point of view about the management of COVID-19 vaccination from Italian experts on IMIDs and the identification of high-risk groups according to the different diseases and their chronic therapy.


Subject(s)
COVID-19 Vaccines/immunology , COVID-19/complications , COVID-19/prevention & control , Immune System Diseases/virology , Vaccination/methods , Diabetes Mellitus/immunology , Diabetes Mellitus/virology , Europe , Expert Testimony , Glomerulonephritis/complications , Glomerulonephritis/immunology , Glomerulonephritis/virology , Humans , Inflammation/immunology , Inflammation/virology , Inflammatory Bowel Diseases/complications , Inflammatory Bowel Diseases/immunology , Inflammatory Bowel Diseases/virology , Lung Diseases/complications , Lung Diseases/immunology , Lung Diseases/virology , Pandemics/prevention & control , Rheumatic Diseases/complications , Rheumatic Diseases/immunology , Rheumatic Diseases/virology , Skin Diseases/complications , Skin Diseases/immunology , Skin Diseases/virology , Uveitis/complications , Uveitis/immunology , Uveitis/virology
8.
Cell ; 184(8): 1990-2019, 2021 04 15.
Article in English | MEDLINE | ID: covidwho-1163481

ABSTRACT

The population is aging at a rate never seen before in human history. As the number of elderly adults grows, it is imperative we expand our understanding of the underpinnings of aging biology. Human lungs are composed of a unique panoply of cell types that face ongoing chemical, mechanical, biological, immunological, and xenobiotic stress over a lifetime. Yet, we do not fully appreciate the mechanistic drivers of lung aging and why age increases the risk of parenchymal lung disease, fatal respiratory infection, and primary lung cancer. Here, we review the molecular and cellular aspects of lung aging, local stress response pathways, and how the aging process predisposes to the pathogenesis of pulmonary disease. We place these insights into context of the COVID-19 pandemic and discuss how innate and adaptive immunity within the lung is altered with age.


Subject(s)
Aging , Cellular Senescence , Lung Diseases , Lung , Adaptive Immunity , Aged , Aging/immunology , Aging/pathology , COVID-19/immunology , COVID-19/pathology , Humans , Lung/immunology , Lung/pathology , Lung Diseases/immunology , Lung Diseases/pathology , Oxidative Stress
9.
Int J Mol Sci ; 22(4)2021 Feb 22.
Article in English | MEDLINE | ID: covidwho-1110433

ABSTRACT

By dint of the aging population and further deepened with the Covid-19 pandemic, lung disease has turned out to be a major cause of worldwide morbidity and mortality. The condition is exacerbated when the immune system further attacks the healthy, rather than the diseased, tissue within the lung. Governed by unremittingly proliferating mesenchymal cells and increased collagen deposition, if inflammation persists, as frequently occurs in aging lungs, the tissue develops tumors and/or turns into scars (fibrosis), with limited regenerative capacity and organ failure. Fas ligand (FasL, a ligand of the Fas cell death receptor) is a key factor in the regulation of these processes. FasL is primarily found in two forms: full length (membrane, or mFasL) and cleaved (soluble, or sFasL). We and others found that T-cells expressing the mFasL retain autoimmune surveillance that controls mesenchymal, as well as tumor cell accumulation following an inflammatory response. However, mesenchymal cells from fibrotic lungs, tumor cells, or cells from immune-privileged sites, resist FasL+ T-cell-induced cell death. The mechanisms involved are a counterattack of immune cells by FasL, by releasing a soluble form of FasL that competes with the membrane version, and inhibits their cell death, promoting cell survival. This review focuses on understanding the previously unrecognized role of FasL, and in particular its soluble form, sFasL, in the serum of aged subjects, and its association with the evolution of lung disease, paving the way to new methods of diagnosis and treatment.


Subject(s)
COVID-19/immunology , Fas Ligand Protein/immunology , Lung Diseases/immunology , Lung/immunology , Age Factors , Aged , COVID-19/blood , Cell Death/immunology , Fas Ligand Protein/blood , Humans , Immunity , Lung Diseases/blood , SARS-CoV-2/immunology , SARS-CoV-2/isolation & purification , T-Lymphocytes/immunology
10.
Int Immunopharmacol ; 94: 107485, 2021 May.
Article in English | MEDLINE | ID: covidwho-1108361

ABSTRACT

The lungs are directly connected to the external environment, which makes them more vulnerable to infection and injury. They are protected by the respiratory epithelium and immune cells to maintain a dynamic balance. Both innate and adaptive immune cells are involved in the pathogenesis of lung diseases. Mucosal-associated invariant T (MAIT) cells are a subset of unconventional T cells, which have attracted increasing attention in recent years. Although MAIT cells account for a small part of the total immune cells in the lungs, evidence suggests that these cells are activated by T cell receptors and/or cytokine receptors and mediate immune response. They play an important role in immunosurveillance and immunity against microbial infection, and recent studies have shown that subsets of MAIT cells play a role in promoting pulmonary inflammation. Emerging data indicate that MAIT cells are involved in the immune response against SARS-CoV-2 and possible immunopathogenesis in COVID-19. Here, we introduce MAIT cell biology to clarify their role in the immune response. Then we review MAIT cells in human and murine lung diseases, including asthma, chronic obstructive pulmonary disease, pneumonia, pulmonary tuberculosis and lung cancer, and discuss their possible protective and pathological effects. MAIT cells represent an attractive marker and potential therapeutic target for disease progression, thus providing new strategies for the treatment of lung diseases.


Subject(s)
Lung Diseases/immunology , Mucosal-Associated Invariant T Cells/immunology , SARS-CoV-2 , Animals , Humans
11.
Oxid Med Cell Longev ; 2021: 6646923, 2021.
Article in English | MEDLINE | ID: covidwho-1093883

ABSTRACT

Inflammatory lung disease results in a high global burden of death and disability. There are no effective treatments for the most severe forms of many inflammatory lung diseases, such as chronic obstructive pulmonary disease, emphysema, corticosteroid-resistant asthma, and coronavirus disease 2019; hence, new treatment options are required. Here, we review the role of oxidative imbalance in the development of difficult-to-treat inflammatory lung diseases. The inflammation-induced overproduction of reactive oxygen species (ROS) means that endogenous antioxidants may not be sufficient to prevent oxidative damage, resulting in an oxidative imbalance in the lung. In turn, intracellular signaling events trigger the production of proinflammatory mediators that perpetuate and aggravate the inflammatory response and may lead to tissue damage. The production of high levels of ROS in inflammatory lung diseases can induce the phosphorylation of mitogen-activated protein kinases, the inactivation of phosphoinositide 3-kinase (PI3K) signaling and histone deacetylase 2, a decrease in glucocorticoid binding to its receptor, and thus resistance to glucocorticoid treatment. Hence, antioxidant treatment might be a therapeutic option for inflammatory lung diseases. Preclinical studies have shown that antioxidants (alone or combined with anti-inflammatory drugs) are effective in the treatment of inflammatory lung diseases, although the clinical evidence of efficacy is weaker. Despite the high level of evidence for the efficacy of antioxidants in the treatment of inflammatory lung diseases, the discovery and clinical investigation of safer, more efficacious compounds are now a priority.


Subject(s)
Antioxidants/therapeutic use , Inflammation/drug therapy , Inflammation/metabolism , Lung Diseases/drug therapy , Lung Diseases/metabolism , Animals , Humans , Inflammation/immunology , Lung/drug effects , Lung/metabolism , Lung Diseases/immunology , Oxidation-Reduction/drug effects , Phosphatidylinositol 3-Kinases/metabolism , Pulmonary Disease, Chronic Obstructive/drug therapy , Pulmonary Disease, Chronic Obstructive/immunology , Pulmonary Disease, Chronic Obstructive/metabolism , Reactive Oxygen Species/metabolism
12.
Crit Care ; 25(1): 53, 2021 02 08.
Article in English | MEDLINE | ID: covidwho-1069578

ABSTRACT

The current pandemic of COVID-19 caused thousands of deaths and healthcare professionals struggle to properly manage infected patients. This review summarizes information about SARS-CoV-2 receptor binding dynamics and intricacies, lung autopsy findings, immune response patterns, evidence-based explanations for the immune response, and COVID-19-associated hypercoagulability.


Subject(s)
COVID-19/physiopathology , Carrier Proteins/physiology , Lung Diseases/physiopathology , Pneumonia, Viral/physiopathology , SARS-CoV-2/pathogenicity , COVID-19/immunology , Carrier Proteins/immunology , Humans , Lung Diseases/immunology , Pandemics , Pneumonia, Viral/immunology , SARS-CoV-2/immunology
13.
Med Hypotheses ; 144: 110043, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-671756

ABSTRACT

HYPOTHESIS: The delayed lung damage after SARS-CoV-2 infection may be caused by an autoimmune response to ACE2 induced by forced presentation of the ACE2 protein in a complex with CoV Spike in Fc Receptor positive Antigen Presenting Cells in the lung. The likelihood that this hypothesis is valid is low, but it is easily tested. TESTABLE PREDICTIONS: 1) Autoantibodies and T cells to ACE2 may be found in patients with the lung damage but not in those without 2) There may be an HLA linkage with the delayed lung disease 3) Vaccines based on the spike protein might initiate the process by amplifying Fc mediated uptake of ACE2-Spike complexes into APCs. PRACTICAL IMPLICATIONS: The development of autoantibodies to ACE2 might predict the development of the inflammatory phase of Covid-19 disease. It might be wise to consider engineering versions of the spike that no longer bind to ACE2 for inclusion in vaccines.


Subject(s)
Angiotensin-Converting Enzyme 2/chemistry , Autoimmunity , COVID-19/immunology , Inflammation/metabolism , Antigen-Presenting Cells/immunology , Autoantibodies/immunology , Binding Sites , COVID-19/virology , HLA Antigens/immunology , Humans , Lung Diseases/immunology , Models, Theoretical , Protein Binding , Protein Domains , Receptors, Fc/immunology , Spike Glycoprotein, Coronavirus/immunology , T-Lymphocytes/immunology , Virus Internalization
15.
J Transl Med ; 18(1): 297, 2020 08 03.
Article in English | MEDLINE | ID: covidwho-692007

ABSTRACT

BACKGROUND: The severe acute respiratory syndrome virus SARS-CoV-2, a close relative of the SARS-CoV virus, is the cause of the recent COVID-19 pandemic affecting, to date, over 14 million individuals across the globe and demonstrating relatively high rates of infection and mortality. A third virus, the H5N1, responsible for avian influenza, has caused infection with some clinical similarities to those in COVID-19 infections. Cytokines, small proteins that modulate immune responses, have been directly implicated in some of the severe responses seen in COVID-19 patients, e.g. cytokine storms. Understanding the immune processes related to COVID-19, and other similar infections, could help identify diagnostic markers and therapeutic targets. METHODS: Here we examine data of cytokine, immune cell types, and disease associations captured from biomedical literature associated with COVID-19, Coronavirus in general, SARS, and H5N1 influenza, with the objective of identifying potentially useful relationships and areas for future research. RESULTS: Cytokine and cell-type associations captured from Medical Subject Heading (MeSH) terms linked to thousands of PubMed records, has identified differing patterns of associations between the four corpuses of publications (COVID-19, Coronavirus, SARS, or H5N1 influenza). Clustering of cytokine-disease co-occurrences in the context of Coronavirus has identified compelling clusters of co-morbidities and symptoms, some of which already known to be linked to COVID-19. Finally, network analysis identified sub-networks of cytokines and immune cell types associated with different manifestations, co-morbidities and symptoms of Coronavirus, SARS, and H5N1. CONCLUSION: Systematic review of research in medicine is essential to facilitate evidence-based choices about health interventions. In a fast moving pandemic the approach taken here will identify trends and enable rapid comparison to the literature of related diseases.


Subject(s)
Betacoronavirus , Coronavirus Infections/immunology , Lung Diseases/immunology , Pneumonia, Viral/immunology , Publications , COVID-19 , Cluster Analysis , Comorbidity , Cytokine Release Syndrome/virology , Cytokines/immunology , Hematopoietic Stem Cells/cytology , Humans , Immune System , Influenza A Virus, H5N1 Subtype , Influenza, Human/immunology , Pandemics , PubMed , SARS-CoV-2 , Severe Acute Respiratory Syndrome/immunology
16.
Clin Immunol ; 218: 108524, 2020 09.
Article in English | MEDLINE | ID: covidwho-639598

ABSTRACT

The outbreak of SARS-CoV-2-associated pneumonia, a disease called COVID-19, has caused a pandemic worldwide. To investigate the immune responses after infection of SARS-CoV-2 in non-critical patients may help to better understand the disease progression. We collected 334 confirmed COVID-19 cases including 212 still in hospital with nucleic acid test positive on halfway for SARS-CoV-2 and 122 discharged from hospital, compared specific antibodies, immune cells, and cytokine changes between the hospitalized and discharged patients. The hospitalized patients had a longer illness time compared with discharged patients. Analysis of viral loads explained long-term or persistent infection of SARS-CoV-2, which existed with the median time of 18.5 days of the positive nucleic acid test. Serum analysis showed that the specific anti-N IgG antibody was positive in all detected patients after infection of two weeks. Neutrophils, Monocytes, NK cells, and CD4+ T cells significantly increased, while total lymphocytes and CD8+ T cells decreased from non-critical hospitalized patients after longer-term infection. Further analysis of the cytokines showed that IL-6, TNF-α, IFN-γ, IL-2, IL-4, and IL-10 from the hospitalized patients were significantly higher, indicating a potential of the increased CD4+ T cell differentiation.


Subject(s)
Betacoronavirus/pathogenicity , Cardiovascular Diseases/immunology , Coronavirus Infections/immunology , Diabetes Mellitus/immunology , Immunity, Innate , Lung Diseases/immunology , Neoplasms/immunology , Pneumonia, Viral/immunology , Aged , Antibodies, Viral/blood , Betacoronavirus/immunology , COVID-19 , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/pathology , Cardiovascular Diseases/virology , China/epidemiology , Comorbidity , Convalescence , Coronavirus Infections/epidemiology , Coronavirus Infections/pathology , Coronavirus Infections/virology , Cytokines/blood , Diabetes Mellitus/epidemiology , Diabetes Mellitus/pathology , Diabetes Mellitus/virology , Female , Hospitalization , Humans , Killer Cells, Natural/immunology , Killer Cells, Natural/pathology , Killer Cells, Natural/virology , Lung Diseases/epidemiology , Lung Diseases/pathology , Lung Diseases/virology , Lymphocyte Subsets/immunology , Lymphocyte Subsets/pathology , Lymphocyte Subsets/virology , Male , Middle Aged , Monocytes/immunology , Monocytes/pathology , Monocytes/virology , Neoplasms/epidemiology , Neoplasms/pathology , Neoplasms/virology , Neutrophils/immunology , Neutrophils/pathology , Neutrophils/virology , Pandemics , Patient Discharge , Pneumonia, Viral/epidemiology , Pneumonia, Viral/pathology , Pneumonia, Viral/virology , SARS-CoV-2 , Time Factors , Viral Load/immunology
17.
mSphere ; 5(3)2020 06 24.
Article in English | MEDLINE | ID: covidwho-616594

ABSTRACT

COVID-19 is often related to hyperinflammation that drives lung or multiorgan injury. The immunopathological mechanisms that cause excessive inflammation are under investigation and constantly updated. Here, a gene network approach was used on recently published data sets to identify possible COVID-19 inflammatory mechanisms and bioactive genes. First, network analysis of putative SARS-CoV-2 cellular receptors led to the mining of a neutrophil-response signature and relevant inflammatory genes. Second, analysis of RNA-seq data sets of lung cells infected with SARS-CoV-2 revealed that infected cells expressed neutrophil-attracting chemokines. Third, analysis of RNA-seq data sets of bronchoalveolar lavage fluid cells from COVID-19 patients identified upregulation of neutrophil genes and chemokines. Different inflammatory genes mined here, including TNFR, IL-8, CXCR1, CXCR2, ADAM10, GPR84, MME, ANPEP, and LAP3, might be druggable targets in efforts to limit SARS-CoV-2 inflammation in severe clinical cases. The possible role of neutrophils in COVID-19 inflammation needs to be studied further.


Subject(s)
Betacoronavirus/immunology , Chemokines/immunology , Coronavirus Infections/immunology , Inflammation/pathology , Neutrophils/immunology , Pneumonia, Viral/immunology , Bronchoalveolar Lavage Fluid/cytology , COVID-19 , Chemokines/genetics , Coronavirus Infections/pathology , Humans , Inflammation/immunology , Lung Diseases/immunology , Lung Diseases/pathology , Neutrophil Infiltration/immunology , Pandemics , Pneumonia, Viral/pathology , Receptors, Virus/genetics , SARS-CoV-2
19.
Cytokine Growth Factor Rev ; 53: 13-24, 2020 06.
Article in English | MEDLINE | ID: covidwho-324437

ABSTRACT

COVID-19 mortality is strongly associated with the development of severe pneumonia and acute respiratory distress syndrome with the worst outcome resulting in cytokine release syndrome and multiorgan failure. It is becoming critically important to identify at the early stage of the infection those patients who are prone to develop the most adverse effects. Elevated systemic interleukin-6 levels in patients with COVID-19 are considered as a relevant parameter in predicting most severe course of disease and the need for intensive care. This review discusses the mechanisms by which IL-6 may possibly contribute to disease exacerbation and the potential of therapeutic approaches based on anti-IL-6 biologics.


Subject(s)
Antibodies, Monoclonal, Humanized/therapeutic use , Coronavirus Infections/drug therapy , Cytokine Release Syndrome/drug therapy , Interleukin-6/antagonists & inhibitors , Pneumonia, Viral/drug therapy , Betacoronavirus/drug effects , Betacoronavirus/immunology , Betacoronavirus/pathogenicity , COVID-19 , Coronavirus Infections/mortality , Coronavirus Infections/pathology , Cytokine Release Syndrome/pathology , Cytokine Release Syndrome/virology , Humans , Interleukin-6/blood , Interleukin-6/immunology , Lung Diseases/immunology , Lung Diseases/pathology , Lung Diseases/virology , Pandemics , Pneumonia, Viral/mortality , Pneumonia, Viral/pathology , SARS-CoV-2
20.
Clin Chim Acta ; 508: 110-114, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-245497

ABSTRACT

BACKGROUND: We observe changes of the main lymphocyte subsets (CD16+CD56、CD19、CD3、CD4、and CD8) in COVID-19-infected patients and explore whether the changes are associated with disease severity. METHODS: One-hundred and fifty-four cases of COVID-19-infected patients were selected and divided into 3 groups (moderate group, severe group and critical group). The flow cytometry assay was performed to examine the numbers of lymphocyte subsets. RESULTS: CD3+, CD4+ and CD8 + T lymphocyte subsets were decreased in COVID-19-infected patients. Compared with the moderate group and the sever group, CD3+, CD4+ and CD8+ T cells in the critical group decreased greatly (P < 0.001, P = 0.005 or P = 0.001). CONCLUSIONS: Reduced CD3+, CD4+, CD8+ T lymphocyte counts may reflect the severity of the COVID-19. Monitoring T cell changes has important implications for the diagnosis and treatment of severe patients who may become critically ill.


Subject(s)
Betacoronavirus/pathogenicity , Cardiovascular Diseases/diagnosis , Coronavirus Infections/diagnosis , Diabetes Mellitus/diagnosis , Lung Diseases/diagnosis , Pneumonia, Viral/diagnosis , T-Lymphocyte Subsets/pathology , Aged , Aged, 80 and over , Biomarkers/analysis , CD3 Complex/genetics , CD3 Complex/immunology , CD4 Antigens/genetics , CD4 Antigens/immunology , CD8 Antigens/genetics , CD8 Antigens/immunology , COVID-19 , Cardiovascular Diseases/immunology , Cardiovascular Diseases/mortality , Cardiovascular Diseases/physiopathology , Cohort Studies , Comorbidity , Coronavirus Infections/immunology , Coronavirus Infections/mortality , Coronavirus Infections/physiopathology , Diabetes Mellitus/immunology , Diabetes Mellitus/mortality , Diabetes Mellitus/physiopathology , Female , Gene Expression , Humans , Immunophenotyping , Lung Diseases/immunology , Lung Diseases/mortality , Lung Diseases/physiopathology , Male , Middle Aged , Pandemics , Patient Selection , Pneumonia, Viral/immunology , Pneumonia, Viral/mortality , Pneumonia, Viral/physiopathology , Prognosis , SARS-CoV-2 , Severity of Illness Index , Survival Analysis , T-Lymphocyte Subsets/immunology , T-Lymphocyte Subsets/virology
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