Cellular Immunity in the Lung

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 18262

Special Issue Editors


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1. Faculty of Health & Life Sciences, Northumbria University, Newcastle upon Tyne NE1 8ST, UK
2. Translational & Clinical Research Institute, The Medical School, Newcastle University, Newcastle upon Tyne NE2 4HH, UK
Interests: T cells; anti-microbial immunity; immune memory; biomarkers
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Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY, USA
Interests: T cells; immunological memory; resident memory; mucosal immunity
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Guest Editor
Department of Life Sciences, Brunel University London, London, UK
Interests: vaccine-induced immunity; tuberculosis; BCG; correlates of protection
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Guest Editor
Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, London, UK
Interests: innate immunity; mucosal immunology; epithelial cell biology; anti-viral immunity
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Special Issue Information

Dear Colleagues,

The role of immune responses in the lung has been brought into sharp focus with the ongoing SARS-CoV-2 pandemic. Numerous microbial pathogens are a threat to lung function and overall health, particularly in those with underlying lung conditions, as well as in people with other risk factors including medical, geographical, and socioeconomic disparities. A fine balance must be achieved in the lung between sufficient immune responses to prevent or clear microbial colonization and/or disease, and the prevention of excessive immune responses that damage the lung and other tissues and organs. Effective immune responses involve innate immunity such as alveolar macrophages, neutrophils, and natural killer cells; and adaptive immune responses including T cells (CD4 and CD8), and B cells/antibodies. However, the precise divide—and relationship—between innate and adaptive immunity is being revealed as far less clear than previously understood. Whilst vaccines are predominantly focused on generating, via injection, adaptive immune responses that are mobile and able to home to the lungs, the need for locally-generated or locally-focused innate and adaptive immune memory is receiving increased attention. Categories of immune responses, including the appropriate cellular effector, memory, homing, and specificity phenotype, are key. This Special Issue of Cells aims to bring together current research and opinion on lung immunity and its role in naturally and artificially/vaccine-generated protective immunity against lung pathogens.

You may choose our Joint Special Issue in JoR.

Prof. Dr. Stephen Todryk
Dr. Joshua Gray
Dr. Steven Smith
Dr. Ryan Thwaites
Guest Editors

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Keywords

  • lung immunity
  • T cells
  • lung infection
  • immunopathology
  • vaccines

Published Papers (3 papers)

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Research

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16 pages, 3387 KiB  
Article
Regulatory and Effector Cell Disequilibrium in Patients with Acute Cellular Rejection and Chronic Lung Allograft Dysfunction after Lung Transplantation: Comparison of Peripheral and Alveolar Distribution
by Laura Bergantini, Miriana d’Alessandro, Elda De Vita, Felice Perillo, Antonella Fossi, Luca Luzzi, Piero Paladini, Anna Perrone, Paola Rottoli, Piersante Sestini, Elena Bargagli and David Bennett
Cells 2021, 10(4), 780; https://doi.org/10.3390/cells10040780 - 01 Apr 2021
Cited by 16 | Viewed by 2267
Abstract
Background: The immune mechanisms occurring during acute rejection (AR) and chronic lung allograft dysfunction are a challenge for research and the balance between effector and regulatory cells has not been defined completely. In this study, we aimed to elucidate the interaction of effector [...] Read more.
Background: The immune mechanisms occurring during acute rejection (AR) and chronic lung allograft dysfunction are a challenge for research and the balance between effector and regulatory cells has not been defined completely. In this study, we aimed to elucidate the interaction of effector cells, mainly Th17, Th1 and Th2, and regulatory cells including (CD4+CD25+CD127low/−) T reg cells and phenotypes of B regs, CD19+CD24hiCD38hi, CD19+CD24hiCD27hi and CD19+CD5+CD1d+. Methods: Bronchoalveolar lavage cells (BAL) and peripheral blood mononuclear cells (PBMCs) from stable lung transplanted (LTx )subjects (n = 4), AR patients (n = 6) and bronchiolitis obliterans syndrome (BOS) (n = 6) were collected at the same time. Cellular subsets were detected through flow cytometry. Results: A predominance of Th17 cells subtypes in the PBMCs and BAL and a depletion of Tregs, that resulted in decrease Treg/Th17 ratio, was observed in the AR group. CD19+CD24hiCD38hi Bregs resulted increased in BAL of AR patients. Th1 cells predominance and a reduction of Tregs cells was observed in BAL from AR patients. Moreover, multivariate analysis showed interdependences within studied variables revealing that effector cells and regulatory cells can effectively discriminate patients’ immunological status. Conclusions: In AR, BOS and stable lung transplant, regulatory and effector cells clearly demonstrated different pathways of activation. Understanding of the balance of T cells and T and B regulatory cells can offers insights into rejection. Full article
(This article belongs to the Special Issue Cellular Immunity in the Lung)
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Review

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24 pages, 1368 KiB  
Review
Mucosal Immune Responses to Respiratory Syncytial Virus
by Megan V. C. Barnes, Peter J. M. Openshaw and Ryan S. Thwaites
Cells 2022, 11(7), 1153; https://doi.org/10.3390/cells11071153 - 29 Mar 2022
Cited by 14 | Viewed by 5183
Abstract
Despite over half a century of research, respiratory syncytial virus (RSV)-induced bronchiolitis remains a major cause of hospitalisation in infancy, while vaccines and specific therapies still await development. Our understanding of mucosal immune responses to RSV continues to evolve, but recent studies again [...] Read more.
Despite over half a century of research, respiratory syncytial virus (RSV)-induced bronchiolitis remains a major cause of hospitalisation in infancy, while vaccines and specific therapies still await development. Our understanding of mucosal immune responses to RSV continues to evolve, but recent studies again highlight the role of Type-2 immune responses in RSV disease and hint at the possibility that it dampens Type-1 antiviral immunity. Other immunoregulatory pathways implicated in RSV disease highlight the importance of focussing on localised mucosal responses in the respiratory mucosa, as befits a virus that is essentially confined to the ciliated respiratory epithelium. In this review, we discuss studies of mucosal immune cell infiltration and production of inflammatory mediators in RSV bronchiolitis and relate these studies to observations from peripheral blood. We also discuss the advantages and limitations of studying the nasal mucosa in a disease that is most severe in the lower airway. A fresh focus on studies of RSV pathogenesis in the airway mucosa is set to revolutionise our understanding of this common and important infection. Full article
(This article belongs to the Special Issue Cellular Immunity in the Lung)
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26 pages, 4030 KiB  
Review
The Role of Epithelial Damage in the Pulmonary Immune Response
by Rachel Ann Burgoyne, Andrew John Fisher and Lee Anthony Borthwick
Cells 2021, 10(10), 2763; https://doi.org/10.3390/cells10102763 - 15 Oct 2021
Cited by 43 | Viewed by 10037
Abstract
Pulmonary epithelial cells are widely considered to be the first line of defence in the lung and are responsible for coordinating the innate immune response to injury and subsequent repair. Consequently, epithelial cells communicate with multiple cell types including immune cells and fibroblasts [...] Read more.
Pulmonary epithelial cells are widely considered to be the first line of defence in the lung and are responsible for coordinating the innate immune response to injury and subsequent repair. Consequently, epithelial cells communicate with multiple cell types including immune cells and fibroblasts to promote acute inflammation and normal wound healing in response to damage. However, aberrant epithelial cell death and damage are hallmarks of pulmonary disease, with necrotic cell death and cellular senescence contributing to disease pathogenesis in numerous respiratory diseases such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and coronavirus disease (COVID)-19. In this review, we summarise the literature that demonstrates that epithelial damage plays a pivotal role in the dysregulation of the immune response leading to tissue destruction and abnormal remodelling in several chronic diseases. Specifically, we highlight the role of epithelial-derived damage-associated molecular patterns (DAMPs) and senescence in shaping the immune response and assess their contribution to inflammatory and fibrotic signalling pathways in the lung. Full article
(This article belongs to the Special Issue Cellular Immunity in the Lung)
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