Maria Tsoumakidou

Alexander Fleming Biomedical Sciences Research Center

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ΝT

Νikolaos Tzanakis

University of Crete

Nikolaos M. Siafakas

University of Crete

Spyros Zakynthinos

Evangelismos Hospital

ΚP

Κonstantinos Potaris

Sotiria General Hospital

Ioanna Tsiligianni

University of Crete

Dimitra Kerdidani

Alexander Fleming Biomedical Sciences Research Center

Georgios Chrysofakis

University of Crete

Izolde Bouloukaki

University of Crete

Peter K. Jeffery

Imperial College London

Eleni Litsiou

Evangelismos Hospital

Cooperative Institutions

National and Kapodistrian University of Athens

Charité - Universitätsmedizin Berlin

University of Crete

German Rheumatism Research Centre

Institute of Immunology

Istituti di Ricovero e Cura a Carattere Scientifico

Heidelberg University

Leibniz Association

Humboldt-Universität zu Berlin

Freie Universität Berlin

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Mechanisms of Altered Cell Immunity and Cytotoxicity in COPD

Current Drug Targets (2011)

Maria Tsoumakidou Ioanna Tsiligianni Νikolaos Tzanakis

The lungs of smokers are exposed to the toxic substances of cigarette smoke, but only 10-20% of them will develop chronic obstructive pulmonary disease (COPD). For COPD to develop, cigarette smoke has to bypass or overwhelm the host front lines of defence, i.e. the respiratory tract mucosal epithelium, which serves as an effective physical barrier and the innate immune system, which provides an immediate, yet non-specific response. In this review, we will describe briefly how cigarette smoke succeeds in damaging the physical barrier of mucosal epithelium and the innate immune system, and how it induces effector mechanisms of the adaptive immune system, which are particularly cytotoxic to the host. We will also discuss the role of other stimuli with immunogenic potential, such of the role of pathogens which colonize or evade the lungs of COPD patients and of self tissue antigens, which may lead to autoimmune disease when there is chronic inflammation. Although the primary mechanism(s) of undesirable innate and adaptive immune responses in COPD are still a matter of debate, it is currently accepted that they are the root cause of COPD.

Cell mediated immunity

10.2174/138945011794751546

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Citations (8)

Novel insights into the aetiology and pathophysiology of increased airway inflammation during COPD exacerbations

Respiratory Research (2006)

Maria Tsoumakidou Nikolaos M. Siafakas

Airway inflammation increases during acute exacerbations of COPD. Extrinsic factors, such as airway infections, increased air pollution, and intrinsic factors, such as increased oxidative stress and altered immunity may contribute to this increase. The evidence for this and the potential mechanisms by which various aetiological agents increase inflammation during COPD exacerbations is reviewed. The pathophysiologic consequences of increased airway inflammation during COPD exacerbations are also discussed. This review aims to establish a cause and effect relationship between etiological factors of increased airway inflammation and COPD exacerbations based on recently published data. Although it can be speculated that reducing inflammation may prevent and/or treat COPD exacerbations, the existing anti-inflammatory treatments are modestly effective.

Pathophysiology

Etiology

10.1186/1465-9921-7-80

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Citations (27)

Interferon-induced lysosomal membrane permeabilization and death cause cDC1-deserts in tumors

bioRxiv (Cold Spring Harbor Laboratory) (2022)

Emmanouil Aerakis A. Chatzigeorgiou Maria V. Alvanou M. Matthaiakaki-Panagiotaki Ilias Angelidis

ABSTRACT T cell immunity requires antigen capture by conventional dendritic cells (cDCs), digestion and transfer to draining lymph nodes for presentation to antigen-inexperienced T cells. cDCs type I excel as cancer-antigen presenting cells, due to their ability to phagocytose, slowly digest apoptotic cancer cells and translocate cancer antigens to the cytosol for loading to MHCI and cross-presentation to CD8 T cells 1–3 . In tumor tissues cDCs1 become particularly scarce and this restricts anti-tumour immunity, immunotherapy responses and patient survival 4–8 . Tumor cDC1 paucity is not fully understood and no specific treatment currently exists. Here, we find that type I interferons (IFN) induce lysosomal stress, lysosomal membrane permeabilization (LMP) and lysosomal-dependent cell death (LDCD) in cDCs1. Two parallel pathways downstream of IFNAR1 converged to induce cDC1 LDCD. Up-regulation of expression of lysosomal genes enhanced the proteolytic activity of lysosomes, while IFN-inducible guanylate binding protein-2 (GBP-2) accumulated in the membrane of the stressed lysosomes, leading to LMP, proteolytic enzyme release and death. Protease inhibition or GBP-2 repression rescued cDCs1 from LDCD and boosted their anti-tumor efficacy. GBPs are amongst the most abundant IFN-induced genes and known to form toxic pores in pathogen-containing vacuoles and pathogen membranes 9 . GBP-2-driven LMP is likely due to the ability of GBP-2 to form pores on the lysosomes of cDC1s. This might have evolved as a physiological mechanism of antigen translocation to the cytosol for cross-presentation 10 . We anticipate our findings to be a starting point for more rational cDC1-directed immunotherapies. For instance, protease inhibition, GBP-2 downregulation or induced expression of LMP repair machinery may boost cDC1 efficacy in adoptive cell therapies or their use as live vaccines 11–13 .

Immunogenic cell death

Cancer Immunotherapy

Antigen processing

10.1101/2022.03.14.484263

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Immunoglobulin-like transcripts 3 (ILT3) expression in human lung adenocarcinoma as a novel regulator of intratumoral lymphoid follicle formation

Lung Cancer (2015)

Vassiliki Karavana Giorgos Kazamias A. Panagiotou Aggeliki Louka Dimitra Kerdidani

10.1183/13993003.congress-2015.pa529

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Citations (1)

Comparison of induced sputum inflammatory profiles between childhood and adult-onset asthma

Respiratory Medicine (2006)

Evangelia Papadopouli Νikolaos Tzanakis Maria Tsoumakidou Despina Kyriakoy Maria Plataki

Atopy

10.1016/j.rmed.2005.11.002

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Citations (13)

Airway Inflammation and Cellular Stress in Noneosinophilic Atopic Asthma

CHEST Journal (2006)

Maria Tsoumakidou Evangelia Papadopouli Νikolaos Tzanakis Nikolaos M. Siafakas

Neutrophil elastase

10.1378/chest.129.5.1194

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Citations (19)

Cigarette Smoking Alters Bronchial Mucosal Immunity in Asthma

American Journal of Respiratory and Critical Care Medicine (2007)

Maria Tsoumakidou William Elston Jie Zhu Zhuo Wang Elizabeth Gamble

Cigarette smoking worsens asthma and is associated with reduced response to corticosteroid therapy. As cigarette smoke is known to have immunomodulatory effects, we hypothesized that one mechanism by which smoking mediates its adverse effect is by reduction of the numbers of bronchial mucosal dendritic cells (DCs), which control B-cell growth and T-cell responses.We set out to sample the bronchial mucosa in smoking and never-smoking patients with asthma and to count DCs, B cells, and cells expressing genes for two key T-lymphocyte regulatory cytokines.Twenty-one never-smoker patients with asthma (6 steroid naive), 24 smoker patients with asthma (9 steroid naive), and 10 healthy never-smokers (control subjects) were recruited and their endobronchial biopsy samples were immunostained for detection of mature DCs (CD83(+)), Langerhans cells (CD1a(+)), B lymphocytes (CD20(+)), and helper T-cell type 1 (IFN-gamma) and helper T-cell type 2 (IL-4) cytokine-expressing cells.The number (per square millimeter) of CD83(+) mature DCs was significantly lower in smoker patients with asthma (median [range]: 37 [0, 131]) in comparison with never-smoker steroid-naive and steroid-treated patients with asthma (76 [24, 464]; p = 0.006) or control subjects (85 [40, 294]; p = 0.004). Moreover, B cells were fewer in smoker (26 [4, 234]) versus never-smoker steroid-naive and steroid-treated patients with asthma (45 [10, 447]; p = 0.01) and in smoker steroid-naive patients with asthma (23 [4, 111]) versus control subjects (34 [10, 130]; p = 0.05). The number of cells expressing IFN-gamma showed a trend toward fewer in smoker (70 [6, 24]) versus never-smoker steroid-naive patients with asthma (144 [44, 323]; p = 0.10).There are important and statistically significant differences in the number of CD83(+) mature DCs and B cells in the large airways of smokers with asthma. We speculate that their reductions may render patients with asthma less responsive to corticosteroids and more susceptible to infection.

10.1164/rccm.200607-908oc

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Citations (80)

Guidelines for the use of flow cytometry and cell sorting in immunological studies (second edition)

European Journal of Immunology (2019)

Andrea Cossarizza Hyun‐Dong Chang Andreas Radbruch Andreas Acs Dieter Adam

These guidelines are a consensus work of a considerable number of members of the immunology and flow cytometry community. They provide the theory and key practical aspects of flow cytometry enabling immunologists to avoid the common errors that often undermine immunological data. Notably, there are comprehensive sections of all major immune cell types with helpful Tables detailing phenotypes in murine and human cells. The latest flow cytometry techniques and applications are also described, featuring examples of the data that can be generated and, importantly, how the data can be analysed. Furthermore, there are sections detailing tips, tricks and pitfalls to avoid, all written and peer-reviewed by leading experts in the field, making this an essential research companion.

Mass cytometry

Cytometry

10.1002/eji.201970107

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Citations (866)

Contents Vol. 150, 2009

International Archives of Allergy and Immunology (2009)

Niels Johansen Richard W. Weber Henrik Ipsen Domingo Barber Louise Broge

10.1159/000259905

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Perforin Expression and Cytotoxic Activity of Sputum CD8 + Lymphocytes in Patients With COPD

CHEST Journal (2004)

George Chrysofakis Νikolaos Tzanakis Despina Kyriakoy Maria Tsoumakidou Ioanna Tsiligianni

10.1378/chest.125.1.71

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Citations (165)