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High levels of lung resident CD4+CD28null cells in COPD: implications of autoimmunity


Hoetzenecker, K; Mitterbauer, A; Guenova, E; Schweiger, T; Altmann, P; Zimmermann, M; Hofbauer, H; Beer, L; Klepetko, W; Ankersmit, H J (2013). High levels of lung resident CD4+CD28null cells in COPD: implications of autoimmunity. Wiener Klinische Wochenschrift, 125(5-6):150-155.

Abstract

Chronic obstructive pulmonary disease (COPD) is a worldwide burden and a major cause of death. Pathogenetic mechanisms underlying the disease are still largely unknown. However, a continuous toxic injury due to tobacco smoking leading to a self-maintaining inflammatory process is considered a key factor in the pathophysiology of the disease. Evidence that autoimmunity might be involved in the maintenance of COPD has been recently noticed with great interest.During the chronic phase of an autoimmune response, lymphocytes lose their costimulatory signals. Previously, CD4+CD28null cells were reported to be systemically heightened in COPD patients. However, a direct role of CD4+CD28null cells in the pathogenesis of COPD is still under discussion, since there is no evidence that CD4+CD28null cells originate from the lungs of diseased patients. Therefore, we evaluated lungs from end-stage COPD patients and compared the levels of tissue infiltrating CD4+CD28null cells to systemic levels. We could show that CD4+CD28null cells are present in high amounts in lung tissue obtained from COPD GOLD IV patients suggesting a direct involvement of those cells in the pathophysiology of COPD. Furthermore, purified lung-resident CD4+ cells showed a stable proliferative response to lung specific elastin and collagen.These results further corroborate the role of autoreactive CD4+ cells in the maintenance of the inflammatory destruction in COPD. Modulating CD4+ cell function might be a new promising tool for future therapeutic approaches.

Abstract

Chronic obstructive pulmonary disease (COPD) is a worldwide burden and a major cause of death. Pathogenetic mechanisms underlying the disease are still largely unknown. However, a continuous toxic injury due to tobacco smoking leading to a self-maintaining inflammatory process is considered a key factor in the pathophysiology of the disease. Evidence that autoimmunity might be involved in the maintenance of COPD has been recently noticed with great interest.During the chronic phase of an autoimmune response, lymphocytes lose their costimulatory signals. Previously, CD4+CD28null cells were reported to be systemically heightened in COPD patients. However, a direct role of CD4+CD28null cells in the pathogenesis of COPD is still under discussion, since there is no evidence that CD4+CD28null cells originate from the lungs of diseased patients. Therefore, we evaluated lungs from end-stage COPD patients and compared the levels of tissue infiltrating CD4+CD28null cells to systemic levels. We could show that CD4+CD28null cells are present in high amounts in lung tissue obtained from COPD GOLD IV patients suggesting a direct involvement of those cells in the pathophysiology of COPD. Furthermore, purified lung-resident CD4+ cells showed a stable proliferative response to lung specific elastin and collagen.These results further corroborate the role of autoreactive CD4+ cells in the maintenance of the inflammatory destruction in COPD. Modulating CD4+ cell function might be a new promising tool for future therapeutic approaches.

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3 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Dermatology Clinic
Dewey Decimal Classification:610 Medicine & health
Language:German
Date:2013
Deposited On:12 Feb 2014 14:02
Last Modified:30 Jun 2016 06:58
Publisher:Springer
ISSN:0043-5325
Publisher DOI:https://doi.org/10.1007/s00508-013-0340-4
PubMed ID:23532603

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