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Article ; Online: Stabilizing human regulatory T cells for tolerance inducing immunotherapy.

He, Xuehui / Koenen, Hans Jpm / Slaats, Jeroen Hr / Joosten, Irma

Immunotherapy

2017 Volume 9, Issue 9, Page(s) 735–751

Abstract: Many autoimmune diseases develop as a consequence of an altered balance between autoreactive immune cells and suppressive ... ...

Abstract	Many autoimmune diseases develop as a consequence of an altered balance between autoreactive immune cells and suppressive FOXP3
Language	English
Publishing date	2017-08
Publishing country	England
Document type	Journal Article
ISSN	1750-7448
ISSN (online)	1750-7448
DOI	10.2217/imt-2017-0017
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Article: Comprehensive phenotyping of circulating immune cell subsets in people living with HIV

Navas, Adriana / Van de Wijer, Lisa / Jacobs-Cleophas, Maartje / Schimmel-Naber, A. Marlies / van Cranenbroek, Bram / van der Heijden, Wouter A. / van der Lei, Roelof J. / Vergara, Zaida / Netea, Mihai G. / van der Ven, André J.A.M. / Kapinsky, Michael / Koenen, Hans J.P.M. / Joosten, Leo A.B.

Journal of immunological methods. 2022 June 21,

2022

Abstract: Systemic chronic inflammation and immune dysfunction are recognized as drivers of the development of non-AIDS related comorbidities (NARCs) in people living with HIV (PLHIV). In order to lower the risk of NARCs, it is critical to elucidate what is the ... ...

Abstract	Systemic chronic inflammation and immune dysfunction are recognized as drivers of the development of non-AIDS related comorbidities (NARCs) in people living with HIV (PLHIV). In order to lower the risk of NARCs, it is critical to elucidate what is the contribution of alterations in the composition and function of circulating immune cells to NARCs-related pathogenesis. Findings from previous immunophenotyping studies in PLHIV are highly heterogeneous and it is not fully understood to what extent phenotypic changes on immune cells play a role in the dysregulated inflammatory response observed. In this study, three flow cytometry panels were designed and standardized to phenotypically and functionally identify the main circulating immune cell subsets in PLHIV. To reduce variability, up to 10 markers out of the approximately 20 markers in each panel were used in a custom dry format DURA Innovations (LUCID product line). Intra-assay precision tests performed for the selected cell subsets showed that the three panels had a %CV below 18% for percent of positive cells and the MFI (mean fluorescent intensity) of lineage markers. Our reported pipeline for immunophenotypic analysis facilitated the discrimination of 1153 cell populations, providing an integrated overview of circulating innate and adaptative immune cells as well as the cells’ functional status in terms of activation, exhaustion, and maturation. When combined with unsupervised computational techniques, this standardized immunophenotyping approach may support the discovery of novel phenotypes with clinical relevance in NARCs and demonstrate future utility in other immune-mediated diseases.
Keywords	flow cytometry ; fluorescence ; functional status ; immunophenotyping ; inflammation ; pathogenesis ; people ; phenotype ; risk
Language	English
Dates of publication	2022-0621
Publishing place	Elsevier B.V.
Document type	Article
Note	Pre-press version
ZDB-ID	120142-6
ISSN	1872-7905 ; 0022-1759
ISSN (online)	1872-7905
ISSN	0022-1759
DOI	10.1016/j.jim.2022.113307
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Chronic HIV infection induces transcriptional and functional reprogramming of innate immune cells.

van der Heijden, Wouter A / Van de Wijer, Lisa / Keramati, Farid / Trypsteen, Wim / Rutsaert, Sofie / Horst, Rob Ter / Jaeger, Martin / Koenen, Hans Jpm / Stunnenberg, Hendrik G / Joosten, Irma / Verweij, Paul E / van Lunzen, Jan / Dinarello, Charles A / Joosten, Leo Ab / Vandekerckhove, Linos / Netea, Mihai G / van der Ven, André Jam / de Mast, Quirijn

JCI insight

2021 Volume 6, Issue 7

Abstract: Chronic inflammation and immune dysfunction play a key role in the development of non-AIDS-related comorbidities. The aim of our study was to characterize the functional phenotype of immune cells in people living with HIV (PLHIV). We enrolled a cross- ... ...

Abstract	Chronic inflammation and immune dysfunction play a key role in the development of non-AIDS-related comorbidities. The aim of our study was to characterize the functional phenotype of immune cells in people living with HIV (PLHIV). We enrolled a cross-sectional cohort study of PLHIV on stable antiretroviral therapy and healthy controls. We assessed ex vivo cytokine production capacity and transcriptomics of monocytes and T cells upon bacterial, fungal, and viral stimulation. PLHIV exhibited an exacerbated proinflammatory profile in monocyte-derived cytokines, but not in lymphocyte-derived cytokines. Particularly, the production of the IL-1β to imiquimod, E. coli LPS, and Mycobacterium tuberculosis was increased, and this production correlated with plasma concentrations of high-sensitivity C-reactive protein and soluble CD14. This increase in monocyte responsiveness remained stable over time in subsequent blood sampling after more than 1 year. Transcriptome analyses confirmed priming of the monocyte IL-1β pathway, consistent with a monocyte-trained immunity phenotype. Increased plasma concentrations of β-glucan, a well-known inducer of trained immunity, were associated with increased innate cytokine responses. Monocytes of PLHIV exhibited a sustained proinflammatory immune phenotype with priming of the IL-1β pathway. Training of the innate immune system in PLHIV likely plays a role in long-term HIV complications and provides a promising therapeutic target for inflammation-related comorbidities.
MeSH term(s)	Adult ; Anti-HIV Agents/therapeutic use ; Case-Control Studies ; Chronic Disease ; Cytokines/genetics ; Cytokines/immunology ; Female ; Gene Expression ; HIV Infections/drug therapy ; HIV Infections/genetics ; HIV Infections/immunology ; Humans ; Immunity, Innate/genetics ; Inflammation/blood ; Inflammation/immunology ; Inflammation/virology ; Interleukin-1beta/blood ; Interleukin-1beta/genetics ; Lipopolysaccharides/pharmacology ; Male ; Middle Aged ; Monocytes/immunology ; Monocytes/virology ; Neutrophils/drug effects ; Neutrophils/immunology ; beta-Glucans/metabolism
Chemical Substances	Anti-HIV Agents ; Cytokines ; IL1B protein, human ; Interleukin-1beta ; Lipopolysaccharides ; beta-Glucans
Language	English
Publishing date	2021-04-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.145928
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Article ; Online: Mature neutrophils and a NF-κB-to-IFN transition determine the unifying disease recovery dynamics in COVID-19.

Frishberg, Amit / Kooistra, Emma / Nuesch-Germano, Melanie / Pecht, Tal / Milman, Neta / Reusch, Nico / Warnat-Herresthal, Stefanie / Bruse, Niklas / Händler, Kristian / Theis, Heidi / Kraut, Michael / van Rijssen, Esther / van Cranenbroek, Bram / Koenen, Hans Jpm / Heesakkers, Hidde / van den Boogaard, Mark / Zegers, Marieke / Pickkers, Peter / Becker, Matthias /

Aschenbrenner, Anna C / Ulas, Thomas / Theis, Fabian J / Shen-Orr, Shai S / Schultze, Joachim L / Kox, Matthijs

Cell reports. Medicine

2022 Volume 3, Issue 6, Page(s) 100652

Abstract: Disease recovery dynamics are often difficult to assess, as patients display heterogeneous recovery courses. To model recovery dynamics, exemplified by severe COVID-19, we apply a computational scheme on longitudinally sampled blood transcriptomes, ... ...

Abstract	Disease recovery dynamics are often difficult to assess, as patients display heterogeneous recovery courses. To model recovery dynamics, exemplified by severe COVID-19, we apply a computational scheme on longitudinally sampled blood transcriptomes, generating recovery states, which we then link to cellular and molecular mechanisms, presenting a framework for studying the kinetics of recovery compared with non-recovery over time and long-term effects of the disease. Specifically, a decrease in mature neutrophils is the strongest cellular effect during recovery, with direct implications on disease outcome. Furthermore, we present strong indications for global regulatory changes in gene programs, decoupled from cell compositional changes, including an early rise in T cell activation and differentiation, resulting in immune rebalancing between interferon and NF-κB activity and restoration of cell homeostasis. Overall, we present a clinically relevant computational framework for modeling disease recovery, paving the way for future studies of the recovery dynamics in other diseases and tissues.
MeSH term(s)	COVID-19 ; Cell Differentiation ; Humans ; Interferons/metabolism ; NF-kappa B/genetics ; Neutrophils/metabolism ; Signal Transduction
Chemical Substances	NF-kappa B ; Interferons (9008-11-1)
Language	English
Publishing date	2022-05-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2022.100652
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Article ; Online: No indications for overt innate immune suppression in critically ill COVID-19 patients

Kox, Matthijs / Frenzel, Tim / Schouten, Jeroen / van de Veerdonk, Frank / Koenen, Hans J.P.M. / Pickkers, Peter / RCI-COVID-19 study group

medRxiv

Abstract: At the end of March 2020, there were in excess of 800.000 confirmed cases of coronavirus disease 2019 (COVID-19) worldwide. Several reports suggest that, in severe cases, COVID-19 may cause a hyperinflammatory 9cytokine storm9. However, unlike SARS-CoV ... ...

Abstract	At the end of March 2020, there were in excess of 800.000 confirmed cases of coronavirus disease 2019 (COVID-19) worldwide. Several reports suggest that, in severe cases, COVID-19 may cause a hyperinflammatory 9cytokine storm9. However, unlike SARS-CoV infection, high levels of anti-inflammatory mediators have also been reported in COVID-19 patients. One study reported that 16% of COVID-19 patients who died developed secondary infection, which might indicate an immune-suppressed state. We explored kinetics of mHLA-DR expression, the most widely used marker of innate immune suppression in critically ill patients, in COVID-19 patients admitted to the ICU. Twenty-four confirmed COVID-19 patients were included, of which 75% was male and 79% had comorbidities. All patients were mechanically ventilated and exhibited large high levels of inflammatory parameters such as CRP and PCT. mHLA-DR expression levels were mostly within the normal range of 15000 - 45000 mAb/cell and showed no change over time. COVID-19 patients displayed notably higher mHLA-DR expression levels compared with bacterial septic shock patients. None of the COVID-19 patients developed a secondary infection. In conclusion, despite a pronounced inflammatory response, mHLA-DR expression kinetics indicate no overt innate immune suppression in COVID-19 patients. These data signify that innate immune suppression as a negative feedback mechanism following PAMP-induced inflammation appears not to be present in COVID-19.
Keywords	covid19
Language	English
Publishing date	2020-04-06
Publisher	Cold Spring Harbor Laboratory Press
Document type	Article ; Online
DOI	10.1101/2020.04.03.20049080
Database	COVID19

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Article ; Online: COVID-19 patients exhibit less pronounced immune suppression compared with bacterial septic shock patients

Kox, Matthijs / Frenzel, Tim / Schouten, Jeroen / van de Veerdonk, Frank / Koenen, Hans J.P.M. / Pickkers, Peter / RCI-COVID-19 study group

medRxiv

Abstract	At the end of March 2020, there were in excess of 800.000 confirmed cases of coronavirus disease 2019 (COVID-19) worldwide. Several reports suggest that, in severe cases, COVID-19 may cause a hyperinflammatory 9cytokine storm9. However, unlike SARS-CoV infection, high levels of anti-inflammatory mediators have also been reported in COVID-19 patients. One study reported that 16% of COVID-19 patients who died developed secondary infection, which might indicate an immune-suppressed state. We explored kinetics of mHLA-DR expression, the most widely used marker of innate immune suppression in critically ill patients, in COVID- 19 patients admitted to the ICU. Twenty-four confirmed COVID-19 patients were included, of which 75% was male and 79% had comorbidities. All patients were mechanically ventilated and exhibited large high levels of inflammatory parameters such as CRP and PCT. Although mHLA-DR expression levels in COVID-19 patients were lower than those observed in healthy subjects, the extent of suppression was less pronounced than observed in bacterial septic shock patients. mHLA-DR expression kinetics revealed no change over time. None of the COVID-19 patients developed a secondary infection. In conclusion, despite a pronounced inflammatory response, mHLA-DR expression kinetics indicate more moderate innate immune suppression in COVID-19 patients compared with bacterial septic shock patients. These data signify that innate immune suppression as a negative feedback mechanism following PAMP-induced inflammation appears less pronounced in COVID-19.
Keywords	covid19
Language	English
Publishing date	2020-04-16
Publisher	Cold Spring Harbor Laboratory Press
Document type	Article ; Online
DOI	10.1101/2020.04.03.20049080
Database	COVID19

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Article ; Online: Molecular pathway profiling of T lymphocyte signal transduction pathways; Th1 and Th2 genomic fingerprints are defined by TCR and CD28-mediated signaling

Smeets Ruben L / Fleuren Wilco WM / He Xuehui / Vink Paul M / Wijnands Frank / Gorecka Monika / Klop Henri / Bauerschmidt Sussane / Garritsen Anja / Koenen Hans JPM / Joosten Irma / Boots Annemieke MH / Alkema Wynand

BMC Immunology, Vol 13, Iss 1, p

2012 Volume 12

Abstract: Abstract Background T lymphocytes are orchestrators of adaptive immunity. Naïve T cells may differentiate into Th1, Th2, Th17 or iTreg phenotypes, depending on environmental co-stimulatory signals. To identify genes and pathways involved in ... ...

Abstract	Abstract Background T lymphocytes are orchestrators of adaptive immunity. Naïve T cells may differentiate into Th1, Th2, Th17 or iTreg phenotypes, depending on environmental co-stimulatory signals. To identify genes and pathways involved in differentiation of Jurkat T cells towards Th1 and Th2 subtypes we performed comprehensive transcriptome analyses of Jurkat T cells stimulated with various stimuli and pathway inhibitors. Results from these experiments were validated in a human experimental setting using whole blood and purified CD4+ Tcells. Results Calcium-dependent activation of T cells using CD3/CD28 and PMA/CD3 stimulation induced a Th1 expression profile reflected by increased expression of T-bet, RUNX3, IL-2, and IFNγ, whereas calcium-independent activation via PMA/CD28 induced a Th2 expression profile which included GATA3, RXRA, CCL1 and Itk. Knock down with siRNA and gene expression profiling in the presence of selective kinase inhibitors showed that proximal kinases Lck and PKCθ are crucial signaling hubs during T helper cell activation, revealing a clear role for Lck in Th1 development and for PKCθ in both Th1 and Th2 development. Medial signaling via MAPkinases appeared to be less important in these pathways, since specific inhibitors of these kinases displayed a minor effect on gene expression. Translation towards a primary, whole blood setting and purified human CD4+ T cells revealed that PMA/CD3 stimulation induced a more pronounced Th1 specific, Lck and PKCθ dependent IFNγ production, whereas PMA/CD28 induced Th2 specific IL-5 and IL-13 production, independent of Lck activation. PMA/CD3-mediated skewing towards a Th1 phenotype was also reflected in mRNA expression of the master transcription factor Tbet, whereas PMA/CD28-mediated stimulation enhanced GATA3 mRNA expression in primary human CD4+ Tcells. Conclusions This study identifies stimulatory pathways and gene expression profiles for in vitro skewing of T helper cell activation. PMA/CD3 stimulation enhances a Th1-like response in an Lck and PKCθ dependent fashion, whereas PMA/CD28 stimulation results in a Th2-like phenotype independent of the proximal TCR-tyrosine kinase Lck. This approach offers a robust and fast translational in vitro system for skewed T helper cell responses in Jurkat T cells, primary human CD4+ Tcells and in a more complex matrix such as human whole blood.
Keywords	Signal transduction pathways ; Gene expression profiling ; T lymphocytes ; Th1 and Th2 development ; Immunologic diseases. Allergy ; RC581-607 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Allergy and Immunology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	570
Language	English
Publishing date	2012-03-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Vitamin D₃ down-regulates proinflammatory cytokine response to Mycobacterium tuberculosis through pattern recognition receptors while inducing protective cathelicidin production

Khoo, Ai-Leng / Chai, Louis Y.A / Koenen, Hans J.P.M / Oosting, Marije / Steinmeyer, Andreas / Zuegel, Ulrich / Joosten, Irma / Netea, Mihai G / van der Ven, André J.A.M

Cytokine. 2011 Aug., v. 55, no. 2

2011

Abstract: A well-known association between vitamin D₃ and infection with Mycobacterium tuberculosis has previously been reported, but little is known regarding the underlying mechanisms. We have investigated how 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃] affects the ... ...

Abstract	A well-known association between vitamin D₃ and infection with Mycobacterium tuberculosis has previously been reported, but little is known regarding the underlying mechanisms. We have investigated how 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃] affects the proinflammatory cytokine production induced by M. tuberculosis. Furthermore, we explored whether 1,25(OH)₂D₃ influence the production of the protective antimycobacterial peptide cathelicidin. Upon in vitro stimulation with M. tuberculosis, 1,25(OH)₂D₃ induced a dose-dependent down-regulation of IL-6, TNFα and IFNγ, while increasing the production of IL-10 in culture supernatant as well as cathelicidin mRNA expression. This effect on cytokine response was not due to modulation of T-helper cell differentiation, as T-bet, GATA3, Foxp3 and ROR-γt mRNA expression remained unaffected. Similarly, 1,25(OH)₂D₃ did not affect suppressor of cytokine signaling (SOCS)1 and SOCS3 mRNA expression. The mechanism whereby 1,25(OH)₂D₃ inhibited the proinflammatory cytokine response was through reduced expression of the pattern recognition receptors (PRR) – TLR2, TLR4, Dectin-1 and mannose receptor, whose mRNA and protein expression were both reduced. The suppression of PRRs could be restored by a VDR antagonist. Upon M. tuberculosis stimulation, 1,25(OH)₂D₃ modulates the balance in cytokine production towards an anti-inflammatory profile by repression of TLR2, TLR4, Dectin-1 and mannose receptor expression, while increasing cathelicidin production. These two effects may have beneficial consequences, by reducing the collateral tissue damage induced by proinflammatory cytokines, while the antibacterial effects of cathelicidin are enhanced.
Keywords	CD4-positive T-lymphocytes ; Mycobacterium tuberculosis ; antagonists ; antibacterial properties ; cell differentiation ; gene expression ; interleukin-10 ; interleukin-6 ; mannose ; protein synthesis ; receptors
Language	English
Dates of publication	2011-08
Size	p. 294-300.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1018055-2
ISSN	1096-0023 ; 1043-4666
ISSN (online)	1096-0023
ISSN	1043-4666
DOI	10.1016/j.cyto.2011.04.016
Database	NAL-Catalogue (AGRICOLA)

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Article: Vitamin D₃ down-regulates proinflammatory cytokine response to Mycobacterium tuberculosis through pattern recognition receptors while inducing protective cathelicidin production

Khoo, Ai-Leng / Chai, Louis Y.A. / Koenen, Hans J.P.M. / Oosting, Marije / Steinmeyer, Andreas / Zuegel, Ulrich / Joosten, Irma / Netea, Mihai G. / van der Ven, André J.A.M.

Cytokine

Volume v. 55,, Issue no. 2

Abstract	A well-known association between vitamin D₃ and infection with Mycobacterium tuberculosis has previously been reported, but little is known regarding the underlying mechanisms. We have investigated how 1,25-dihydroxyvitamin D₃ [1,25(OH)₂D₃] affects the proinflammatory cytokine production induced by M. tuberculosis. Furthermore, we explored whether 1,25(OH)₂D₃ influence the production of the protective antimycobacterial peptide cathelicidin. Upon in vitro stimulation with M. tuberculosis, 1,25(OH)₂D₃ induced a dose-dependent down-regulation of IL-6, TNFα and IFNγ, while increasing the production of IL-10 in culture supernatant as well as cathelicidin mRNA expression. This effect on cytokine response was not due to modulation of T-helper cell differentiation, as T-bet, GATA3, Foxp3 and ROR-γt mRNA expression remained unaffected. Similarly, 1,25(OH)₂D₃ did not affect suppressor of cytokine signaling (SOCS)1 and SOCS3 mRNA expression. The mechanism whereby 1,25(OH)₂D₃ inhibited the proinflammatory cytokine response was through reduced expression of the pattern recognition receptors (PRR) – TLR2, TLR4, Dectin-1 and mannose receptor, whose mRNA and protein expression were both reduced. The suppression of PRRs could be restored by a VDR antagonist. Upon M. tuberculosis stimulation, 1,25(OH)₂D₃ modulates the balance in cytokine production towards an anti-inflammatory profile by repression of TLR2, TLR4, Dectin-1 and mannose receptor expression, while increasing cathelicidin production. These two effects may have beneficial consequences, by reducing the collateral tissue damage induced by proinflammatory cytokines, while the antibacterial effects of cathelicidin are enhanced.
Keywords	protein synthesis ; mannose ; interleukin-10 ; CD4-positive T-lymphocytes ; gene expression ; antibacterial properties ; receptors ; antagonists ; cell differentiation ; interleukin-6 ; Mycobacterium tuberculosis
Language	English
Document type	Article
ISSN	1043-4666
Database	AGRIS - International Information System for the Agricultural Sciences and Technology

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