Oligoclonal CD4<sup>+</sup>T Cells in the Lungs of Patients with Severe Emphysema

Sullivan, Andrew; Simonian, Philip L.; Falta, Michael T.; Mitchell, John D.; Cosgrove, Gregory P.; Brown, Kevin K.; Kotzin, Brian L.; Voelkel, Norbert F.; Fontenot, Andrew P.

doi:10.1164/rccm.200410-1332oc

Cited by 140 publications

(110 citation statements)

References 35 publications

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“…The cellular composition varies between individuals, but typically includes neutrophils, macrophages and CD8+ T cells. There are also smaller numbers of CD4+ T cells, but these may be monoclonal (76), and limited to pulmonary follicles (77). Consistently, research has highlighted the importance of the neutrophil in the pathogenesis of COPD and chronic bronchitis.…”

Section: Immunology and Inflammation In Chronic Bronchitismentioning

confidence: 89%

The Importance of Chronic Bronchitis in Chronic Obstructive Pulmonary Disease

Sapey¹,

Stockley²

2011

Bronchitis

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Section: Immunology and Inflammation In Chronic Bronchitismentioning

confidence: 89%

The Importance of Chronic Bronchitis in Chronic Obstructive Pulmonary Disease

Sapey¹,

Stockley²

2011

Bronchitis

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“…This fi nding was echoed by Korn et al who further showed that clonal expansions were most particularly pronounced among CD8 + T-lymphocytes, in both the lung and in the blood of chronic smokers (Korn et al 2005). Additionally, circulating T-lymphocytes and those isolated from COPD lungs frequently exhibit down-regulation of CD28, a co-stimulatory molecule, which, in turn, is another, if less immediately evident consequence of chronic antigen exposure and repeated cell divisions (Sullivan et al 2005). CD28 down-regulation has been documented in a number of chronic infl ammatory syndromes including autoimmune diseases (Schirmer et al 1998) and lung allograft rejection (Studer et al 2008).…”

Section: Peptide Antigens -Triggers Of Adaptive Immune Activationmentioning

confidence: 89%

“…Sullivan et al examined T-lymphocytes isolated from emphysematous lung tissue and demonstrated these populations were comprised of oligoclonal T-cells (Sullivan et al 2005). This fi nding was echoed by Korn et al who further showed that clonal expansions were most particularly pronounced among CD8 + T-lymphocytes, in both the lung and in the blood of chronic smokers (Korn et al 2005).…”

Section: Peptide Antigens -Triggers Of Adaptive Immune Activationmentioning

confidence: 98%

“…Pulmonary lymphocytes isolated from emphysematous lung tissue are frequently activated (Sullivan et al 2005) and capable of secreting mediators that have been implicated in the pathogenesis of COPD (Grumelli et al 2004). T-cells transit between infl ammatory foci in organs and regional lymph nodes, and at least some proportion of these disease-specifi c lymphocytes also traffi c within lymphatic and blood circulations (Lehmann et al 2001).…”

Section: Associations Of T-lymphocytes With Copdmentioning

confidence: 99%

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Role of T-lymphocytes and pro-inflammatory mediators in the pathogenesis of chronic obstructive pulmonary disease

Gadgil

Duncan

2008

COPD

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Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the US and a major worldwide healthcare problem. The pathophysiologic mechanisms that drive development and progression of this disease are complex and only poorly understood. While tobacco smoking is the primary risk factor, other disease processes also appear to play a role. Components of the innate immune system (eg, macrophages and neutrophils) have long been believed to be important in the development of COPD. More recent evidence also suggests involvement of the adaptive immune system in pathogenesis of this disease. Here we will review the literature supporting the participation of T-cells in the development of COPD, and comment on the potential antigenic stimuli that may account for these responses. We will further explore the prospective contributions of T-cell derived mediators that could contribute to the infl ammation, alveolar wall destruction, and small airway fi brosis of advanced COPD. A better understanding of these complex immune processes will lead to new insights that could result in improved preventative and/or treatment strategies.

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“…+ lymphocytes (Sullivan et al, 2005). These findings point to a possible immune mechanism of lung inflammation in COPD (Willemse et al, 2005).…”

Section: Cytotoxic T Lymphocytesmentioning

confidence: 66%

The role of oxidative stress in lung injury induced by cigarette smoke

Kluchová

Tkáčová

2006

Biologia

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Oxidative stress is a damaging process resulting from an imbalance between excessive generation of oxidant compounds and insufficient antioxidant defence mechanisms. Oxidative stress plays a crucial role in the initiation and progression of cigarette smoke-induced lung injury, deterioration in lung functions, and development of chronic obstructive pulmonary disease (COPD). In smokers and in patients with COPD, the increased oxidant burden derives from cigarette smoke per se, and from activated inflammatory cells releasing enhanced amounts of reactive oxygen and nitrogen species (ROS, RNS, respectively). Although mild oxidative stress resulting from cigarette smoking leads to the upregulation of the antioxidative enzymes synthesis in the lungs, high levels of ROS and RNS observed in patients with COPD overwhelm the antioxidant enzymes capacities, resulting in oxidant-mediated lung injury and cell death. In addition, depletion of antioxidative systems in the systemic circulation was consistently observed in such patients. The imbalance between the generation of ROS/RNS and antioxidant capacities -the state of "oxidative stress" -is one of the major pathophysiologic hallmarks in the development of COPD. Detrimental effects of oxidative stress include impairment of membrane functions, inactivation of membrane-bound receptors and enzymes, and increased tissue permeability. In addition, oxidative stress aggravates the inflammatory processes in the lungs, and contributes to the worsening of the protease-antiprotease imbalance. Several markers of oxidative stress, such as increases in lipid peroxidation products and reductions in glutathione peroxidase activity, have been shown to be related to the reductions in pulmonary functions. In the present article we review the current knowledge about the vicious cycle of cigarette smoking, oxidative stress, and inflammation in the pathogenesis of COPD.

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Oligoclonal CD4⁺T Cells in the Lungs of Patients with Severe Emphysema

Cited by 140 publications

References 35 publications

The Importance of Chronic Bronchitis in Chronic Obstructive Pulmonary Disease

The Importance of Chronic Bronchitis in Chronic Obstructive Pulmonary Disease

Role of T-lymphocytes and pro-inflammatory mediators in the pathogenesis of chronic obstructive pulmonary disease

The role of oxidative stress in lung injury induced by cigarette smoke

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Oligoclonal CD4+T Cells in the Lungs of Patients with Severe Emphysema

Cited by 140 publications

References 35 publications

The Importance of Chronic Bronchitis in Chronic Obstructive Pulmonary Disease

The Importance of Chronic Bronchitis in Chronic Obstructive Pulmonary Disease

Role of T-lymphocytes and pro-inflammatory mediators in the pathogenesis of chronic obstructive pulmonary disease

The role of oxidative stress in lung injury induced by cigarette smoke

Contact Info

Product

Resources

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Oligoclonal CD4⁺T Cells in the Lungs of Patients with Severe Emphysema