Helmholtz Munich

Human heart with vessels, lungs, bronchial tree and cut rib cage.

Immunopathology of COPD

We want to understand which subtypes of T-cell play a role in the development of COPD - a major public health problem with prevalence as well as mortality still rising.

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Graphic illustration of alveoli with COPD

The stimulus of long-term exposure to toxic gases and most often cigarette smoke causes parenchymal lung tissue damage, remodeling of small airways, airway obstruction, and a subsequent decline in lung function. Innate inflammatory immune cells, i.e. neutrophils and macrophages, and CD8+ T cells have been described to be considerably involved in lung tissue damage in COPD. However, increasing evidence suggests that the inflammatory response of other specific immune cells, in particular CD4+ T and B cells present in the lungs of COPD patients, contributes to the pathogenesis of COPD. More studies are needed to understand the exact role and involvement of these immune cells in the chronic inflammatory response in COPD.

In COPD, immune cells (B-cells and T-cells) form newly organized structures in the lung, follicles, which are known to play an important role in the disease progression. The formation of these structures requires the activation of a specific cellular receptor: the lymphotoxin beta receptor which is also a regulator of cell death. The death of epithelial lung cells is another feature of COPD observed in patients, preventing them from breathing effectively. We found that the blocking of lymphotoxin beta receptor signaling leads to the activation of so-called Wnt signaling. Wnt signaling is an essential pathway for lung development. In COPD patients this pathway gets switched off preventing the lung from being able to repair and regenerate.

Our work published in Nature journal offers great potential for implementing lung regenerative medicine approaches in the clinic. To achieve this ultimate goal we are testing the novel dual therapeutic approach in human clinical trials over the coming years. (See "Clinical Trials")

PhD Student

2023 European Respiratory Journal

Thomas M Conlon, Ali Önder Yildirim

Oxysterol metabolism dictates macrophage influx during SARS-CoV-2 infection

2022 Nature Communications

Gizem Günes Günsel, Thomas M. Conlon, Aicha Jeridi et al.

The arginine methyltransferase PRMT7 promotes extravasation of monocytes resulting in tissue injury in COPD

2022 Nature Communications

Barbara Spix et al.

Lung emphysema and impaired macrophage elastase clearance in mucolipin 3 deficient mice

2020 Nature

Thomas M. Conlon et al.

Inhibition of LTβR signalling activates WNT-induced regeneration in lung | Nature

2018 EMBO Mol. Med.

Jie Jia et al.

Cholesterol metabolism promotes B-cell positioning during immune pathogenesis of chronic obstructive pulmonary disease

Yildirim/Conlon Lab

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COPD - third leading cause of death worldwide

Promising therapeutic approach against COPD

Scientists at Yildirim/Conlon Lab

Rebecca Bake

Sonja Borndörfer

Kübra Caglar

Sirui Chen

Deepesh Dhakad

Guilherme Dragunas

Dr. Chiara Goracci

Güney Güvenç

Simona Havristiuc

Christine Hollauer

Henri Hoppe

Aylin Housni

Dr. Aicha Jeridi

Dr. Shruthi Kalgudde Gopal

Nele Keuper

Markus Klotz

Dr. Varun Kumar

Elif Ölken Akova

Dr. Neha Patil

Xiaomei Tan

Claas Tapken

Lea Theilacker

Dr. Henu Kumar Verma

Marie Zöller

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Prof. Dr. Ali Önder Yildirim

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Dr. Thomas Conlon

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