At the Checkpoint: Lung CD8<sup>+</sup> T Cells, Respiratory Viruses, and Chronic Obstructive Pulmonary Disease

Curtis, Jeffrey L.

doi:10.1164/rccm.201511-2122ed

Cited by 4 publications

(8 citation statements)

References 15 publications

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“…Therefore adaptive immune responses are carefully regulated to prevent excessive cell damage. 12 An action of air pollution PM to further increase pro-inflammatory cytokine production by CD8 T lymphocytes responding to a viral infection may be detrimental by increasing bystander damage and pathological inflammation. Indeed, pathological CD8 T-lymphocyte responses are increasingly thought to contribute to lung damage in COPD.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, pathological CD8 T-lymphocyte responses are increasingly thought to contribute to lung damage in COPD. 12,46 For example, Makris et al found an increased frequency of CD8 T lymphocytes in induced sputum from COPD patients at the time of exacerbation, interestingly with a decreased frequency of CD4 T lymphocytes at exacerbation. 47 Similarly CD8 T-lymphocyte responses may contribute to pathology in asthma.…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, increased pollution exposure has been associated with exacerbations of chronic obstructive pulmonary disease (COPD),10, 11 a disease characterized by enhanced susceptibility to respiratory viruses12 and infection‐driven airway inflammation 13…”

Section: Introductionmentioning

confidence: 99%

“…CD8 T lymphocytes are of prime importance in anti‐viral adaptive immunity,12, 20, 21, 22 yet the effect of UPM on DC‐stimulated CD8 responses has not been similarly studied. CD8 T lymphocytes employ several mechanisms to kill infected or malignant cells: secretion of cytokines such as IFN‐ γ and tumour necrosis factor‐ α (TNF‐ α ) that have downstream anti‐viral effects, and the production and release of cytotoxic granules containing perforin and granzymes.…”

Section: Introductionmentioning

confidence: 99%

“…Exposures to elevated concentrations of ambient particulate matter (PM) have been shown to be associated with increased asthma exacerbations [1][2][3][4] and viral upper respiratory tract infections [5][6][7] these may be linked as most asthma exacerbations are triggered by upper viral respiratory tract infections. 8,9 Similarly, increased pollution exposure has been associated with exacerbations of chronic obstructive pulmonary disease (COPD), 10,11 a disease characterized by enhanced susceptibility to respiratory viruses 12 and infection-driven airway inflammation. 13 Dendritic cells (DCs) play a major role in orchestrating immune responses in the lungs 14,15 and extensive research has studied the effects of urban particulate matter (UPM) on DC-stimulated CD4 T-lymphocyte responses.…”

Section: Introductionmentioning

confidence: 99%

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Urban particulate matter stimulation of human dendritic cells enhances priming of naive CD8 T lymphocytes

Pfeffer

Mann

et al. 2017

Immunology

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SummaryEpidemiological studies have consistently shown associations between elevated concentrations of urban particulate matter (UPM) air pollution and exacerbations of asthma and chronic obstructive pulmonary disease, which are both associated with viral respiratory infections. The effects of UPM on dendritic cell (DC) ‐stimulated CD4 T lymphocytes have been investigated previously, but little work has focused on CD8 T‐lymphocyte responses despite their importance in anti‐viral immunity. To address this, we examined the effects of UPM on DC‐stimulated naive CD8 T‐cell responses. Expression of the maturation/activation markers CD83, CCR7, CD40 and MHC class I on human myeloid DCs (mDCs) was characterized by flow cytometry after stimulation with UPM in vitro in the presence/absence of granulocyte–macrophage colony‐stimulating factor (GM‐CSF). The capacity of these mDCs to stimulate naive CD8 T‐lymphocyte responses in allogeneic co‐culture was then assessed by measuring T‐cell cytokine secretion using cytometric bead array, and proliferation and frequency of interferon‐γ (IFN‐γ)‐producing T lymphocytes by flow cytometry. Treatment of mDCs with UPM increased expression of CD83 and CCR7, but not MHC class I. In allogeneic co‐cultures, UPM treatment of mDCs enhanced CD8 T‐cell proliferation and the frequency of IFN‐γ + cells. The secretion of tumour necrosis factor‐α, interleukin‐13, Granzyme A and Granzyme B were also increased. GM‐CSF alone, and in concert with UPM, enhanced many of these T‐cell functions. The PM‐induced increase in Granzyme A was confirmed in a human experimental diesel exposure study. These data demonstrate that UPM treatment of mDCs enhances priming of naive CD8 T lymphocytes and increases production of pro‐inflammatory cytokines. Such UPM‐induced stimulation of CD8 cells may potentiate T‐lymphocyte cytotoxic responses upon concurrent airway infection, increasing bystander damage to the airways.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Urban particulate matter stimulation of human dendritic cells enhances priming of naive CD8 T lymphocytes

Pfeffer

Mann

et al. 2017

Immunology

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Immunodeficiency in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease

et al. 2018

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Chronic obstructive pulmonary disease (COPD), characterized by progressive airway inflammation and irreversible airflow limitation, leads to serious decline in life quality. The acute exacerbation of COPD (AECOPD) results in high healthcare costs as well as a significant mortality rate. The most common cause of acute exacerbation is infection. Immune deficiency, which induces dysfunction of anti-infection, plays an important role in the pathogenesis of acute exacerbation. As described in this review, the immune dysfunction in patients with AECOPD can be a major focus of efforts to therapeutic strategy.

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Respiratory viral infection: a potential “missing link” in the pathogenesis of COPD

et al. 2019

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Chronic obstructive pulmonary disease (COPD) is currently the third most common cause of global mortality. Acute exacerbations of COPD frequently necessitate hospital admission to enable more intensive therapy, incurring significant healthcare costs. COPD exacerbations are also associated with accelerated lung function decline and increased risk of mortality. Until recently, bacterial pathogens were believed to be responsible for the majority of disease exacerbations. However, with the advent of cultureindependent molecular diagnostic techniques it is now estimated that viruses are detected during half of all COPD exacerbations and are associated with poorer clinical outcomes. Human rhinovirus, respiratory syncytial virus and influenza are the most commonly detected viruses during exacerbation. The role of persistent viral infection (adenovirus) has also been postulated as a potential pathogenic mechanism in COPD. Viral pathogens may play an important role in driving COPD progression by acting as triggers for exacerbation and subsequent lung function decline whilst the role of chronic viral infection remains a plausible hypothesis that requires further evaluation. There are currently no effective antiviral strategies for patients with COPD. Herein, we focus on the current understanding of the cellular and molecular mechanisms of respiratory viral infection in COPD.

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At the Checkpoint: Lung CD8⁺ T Cells, Respiratory Viruses, and Chronic Obstructive Pulmonary Disease

Cited by 4 publications

References 15 publications

Urban particulate matter stimulation of human dendritic cells enhances priming of naive CD8 T lymphocytes

Urban particulate matter stimulation of human dendritic cells enhances priming of naive CD8 T lymphocytes

Immunodeficiency in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease

Respiratory viral infection: a potential “missing link” in the pathogenesis of COPD

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At the Checkpoint: Lung CD8+ T Cells, Respiratory Viruses, and Chronic Obstructive Pulmonary Disease

Cited by 4 publications

References 15 publications

Urban particulate matter stimulation of human dendritic cells enhances priming of naive CD8 T lymphocytes

Urban particulate matter stimulation of human dendritic cells enhances priming of naive CD8 T lymphocytes

Immunodeficiency in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease

Respiratory viral infection: a potential “missing link” in the pathogenesis of COPD

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Product

Resources

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At the Checkpoint: Lung CD8⁺ T Cells, Respiratory Viruses, and Chronic Obstructive Pulmonary Disease