2024-03-28T21:58:21Zhttp://repository.helmholtz-hzi.de/oai/requestoai:repository.helmholtz-hzi.de:10033/6219702021-07-05T15:12:59Zcom_10033_620652com_10033_620591com_10033_622921col_10033_622922col_10033_620666col_10033_620724
Zheng, Xiaoyan
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500
Oduro, Jennifer D
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500
Boehme, Julia D
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Borkner, Lisa
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500
Ebensen, Thomas
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500
Heise, Ulrike
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500
Gereke, Marcus
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500
Pils, Marina C
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500
Krmpotic, Astrid
ae0c6a8bc5bedc9206b08b9db175429f
500
Guzmán, Carlos A
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Bruder, Dunja
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Čičin-Šain, Luka
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500
HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.
2019-10-09T11:14:24Z
2019-10-09T11:14:24Z
2019-09-01
PLoS Pathog. 2019 Sep 16;15(9):e1008036. doi: 10.1371/journal.ppat.1008036. eCollection 2019 Sep.
1553-7374
31525249
10.1371/journal.ppat.1008036
http://hdl.handle.net/10033/621970
PLOS pathogens
Cytomegalovirus (CMV) is a ubiquitous β-herpesvirus that establishes life-long latent infection in a high percentage of the population worldwide. CMV induces the strongest and most durable CD8+ T cell response known in human clinical medicine. Due to its unique properties, the virus represents a promising candidate vaccine vector for the induction of persistent cellular immunity. To take advantage of this, we constructed a recombinant murine CMV (MCMV) expressing an MHC-I restricted epitope from influenza A virus (IAV) H1N1 within the immediate early 2 (ie2) gene. Only mice that were immunized intranasally (i.n.) were capable of controlling IAV infection, despite the greater potency of the intraperitoneally (i.p.) vaccination in inducing a systemic IAV-specific CD8+ T cell response. The protective capacity of the i.n. immunization was associated with its ability to induce IAV-specific tissue-resident memory CD8+ T (CD8TRM) cells in the lungs. Our data demonstrate that the protective effect exerted by the i.n. immunization was critically mediated by antigen-specific CD8+ T cells. CD8TRM cells promoted the induction of IFNγ and chemokines that facilitate the recruitment of antigen-specific CD8+ T cells to the lungs. Overall, our results showed that locally applied MCMV vectors could induce mucosal immunity at sites of entry, providing superior immune protection against respiratory infections.
en
PLOS
Attribution-NonCommercial-ShareAlike 4.0 International
http://creativecommons.org/licenses/by-nc-sa/4.0/
Mucosal CD8+ T cell responses induced by an MCMV based vaccine vector confer protection against influenza challenge.
Article
PLoS pathogens
2019-10-09T11:14:25Z
THUMBNAIL
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LICENSE
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ORIGINAL
Zheng et al.pdf
Zheng et al.pdf
Open Access publication
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10033/621970
oai:repository.helmholtz-hzi.de:10033/621970
2021-07-05 15:12:59.101
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/6221712020-12-01T14:30:26Zcom_10033_620652com_10033_311308com_10033_620591col_10033_620666col_10033_620724col_10033_620721
Böning, Martha A L
1f4e4cae2c56dbc636f7c6293e8904d4
300
Trittel, Stephanie
1ab2bb099ea32cb74e47a2308a5e1319
500
Riese, Peggy
8c4f5faa7786444779b9cc589e124eb2
600
http://orcid.org/0000-0001-6796-6780
van Ham, Marco
702d5515ad73f4b2c2641e71a6c815a2
500
Heyner, Maxi
eb62538306dafd7c5be591d6bb32694d
500
Voss, Martin
2dab7f8d1b582d4109a280bfcccafa0d
500
Parzmair, Gerald P
a781bb569a5bfa0f52534e44113a0c3b
300
Klawonn, Frank
da2644d10297b6bb437e1cce18952393
600
http://orcid.org/0000-0001-9613-182X
Jeron, Andreas
2a74a8f4c70f434de4f2c7e67bb547ab
500
Guzman, Carlos A
1dc6fd50b3a3354f74ef8672c521d5c7
500
Jänsch, Lothar
14cc18542edf57a7b25c4b0c14a8c05a
600
http://orcid.org/0000-0002-5655-1181
Schraven, Burkhart
732f0e20e2b7411a1d421c8cfd71d687
500
Reinhold, Annegret
0728929609f9eb3457292008f6f4f0e6
500
Bruder, Dunja
1ba4133d9ea07fbb30b11e97f4ab5bda
500
HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.
2020-02-26T08:58:18Z
2020-02-26T08:58:18Z
2019-01-01
Front Immunol. 2020 Jan 22;10:3144. doi: 10.3389/fimmu.2019.03144. eCollection 2019.
1664-3224
32038647
10.3389/fimmu.2019.03144
http://hdl.handle.net/10033/622171
Frontiers of Immunology
The adhesion and degranulation-promoting adaptor protein (ADAP) serves as a multifunctional scaffold and is involved in the formation of immune signaling complexes. To date only limited and moreover conflicting data exist regarding the role of ADAP in NK cells. To extend existing knowledge we investigated ADAP-dependency of NK cells in the context of in vivo infection with the intracellular pathogen Listeria monocytogenes (Lm). Ex vivo analysis of infection-primed NK cells revealed impaired cytotoxic capacity in NK cells lacking ADAP as indicated by reduced CD107a surface expression and inefficient perforin production. However, ADAP-deficiency had no global effect on NK cell morphology or intracellular distribution of CD107a-containing vesicles. Proteomic definition of ADAPko and wild type NK cells did not uncover obvious differences in protein composition during the steady state and moreover, similar early response patterns were induced in NK cells upon infection independent of the genotype. In line with protein network analyses that suggested an altered migration phenotype in naïve ADAPko NK cells, in vitro migration assays uncovered significantly reduced migration of both naïve as well as infection-primed ADAPko NK cells compared to wild type NK cells. Notably, this migration defect was associated with a significantly reduced expression of the integrin CD11a on the surface of splenic ADAP-deficient NK cells 1 day post-Lm infection. We propose that ADAP-dependent alterations in integrin expression might account at least in part for the fact that during in vivo infection significantly lower numbers of ADAPko NK cells accumulate in the spleen i.e., the site of infection. In conclusion, we show here that during systemic Lm infection in mice ADAP is essential for efficient cytotoxic capacity and migration of NK cells.
en
Frontiers
Attribution-NonCommercial-ShareAlike 4.0 International
http://creativecommons.org/licenses/by-nc-sa/4.0/
ADAP
CD11a
IL-10
Listeria monocytogenes
cytotoxicity
in vivo infection
migration
natural killer cells
ADAP Promotes Degranulation and Migration of NK Cells Primed During vivo Listeria monocytogenes Infection in Mice.
Article
Frontiers in immunology
2020-02-26T08:58:19Z
THUMBNAIL
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Open Access publication
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10033/622171
oai:repository.helmholtz-hzi.de:10033/622171
2020-12-01 14:30:26.014
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/6223422020-07-03T01:31:20Zcom_10033_620591col_10033_620724
Veluswamy, Priya
855901d3d994c0c97f54485cc6231f45
300
Bruder, Dunja
b5a4f0fe11461388fa1e79487e3fb00e
600
http://orcid.org/0000-0003-3066-189X
HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.
2020-07-02T13:11:02Z
2020-07-02T13:11:02Z
2018-04
2218-676X
10.21037/tcr.2018.04.04
http://hdl.handle.net/10033/622342
2219-6803
Translational Cancer Research
T cell exhaustion is a well-known mechanism involved in escape of degenerated cells or certain pathogens from CD8+ T cell-mediated immune surveillance, ultimately resulting in tumor development and chronic infections, respectively. Next to activated T cells, exhausted CD8+ T cells typically express high levels of the programmed cell death-1 (PD-1) receptor. While interaction of PD-1 with its ligand programmed death-ligand 1 (PD-L1) on hemotopoietic and non-hemotopoietic cells is important for the re-establishment of homeostasis following immune activation, PD-1/PD-L1 interaction represents a major drawback in certain other disease settings such as cancer or chronic viral infections. Here PD-1 signalling in T cells prevents efficient anti-tumor or anti-viral immune responses. Thus, therapeutic interference with the PD-1/PD-L1 pathway represents a promising approach for releasing exhausted CD8+ T cells from PD-1-dependent suppression and reactivation of effector functions. However, recent reports have highlighted unexpected outcomes of PD-1/PD-L1 pathway inhibition in the context of chronic infections. We provide here a comprehensive overview of the recent discoveries made in the context of PD-1/PD-L1 checkpoint inhibition that are considered relevant with respect to the targeted reactivation of effector functions in exhausted CD8+ T cells. We briefly discuss the impact of PD-1 signalling on the expression of certain transcription factors, on epigenetic modifications affecting chromatin accessibility, on cellular metabolism and the expression of certain cytokine receptors involved in immune homeostasis. These newly uncovered facts should be carefully considered before further development of therapies targeting the PD-1/PD-L1 pathway that are aiming at the restoration of pathogen-specific and anti-tumor CD8+ T cell effector functions in order to prevent adverse side effects. © 2018, Translational Cancer Research.
en
AME Publishing Company
Attribution-NonCommercial-ShareAlike 4.0 International
http://creativecommons.org/licenses/by-nc-sa/4.0/
PD-1/PD-L1 pathway inhibition to restore effector functions in exhausted CD8+ T cells: chances, limitations and potential risks
Article
7
S4
S530
S537
Translational Cancer Research
2020-07-02T13:11:04Z
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Veluswamy and Bruder.pdf
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10033/622342
oai:repository.helmholtz-hzi.de:10033/622342
2020-07-03 01:31:20.443
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/6223432020-07-08T03:31:26Zcom_10033_620591com_10033_620652col_10033_620666col_10033_620724
Stegemann-Koniszewski, Sabine
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Behrens, Sarah
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http://orcid.org/0000-0001-6796-6780
Guzmán, Carlos A
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Kröger, Andrea
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Schreiber, Jens
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Gunzer, Matthias
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Bruder, Dunja
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ZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.
2020-07-07T11:37:39Z
2020-07-07T11:37:39Z
2018-02-13
Front Immunol. 2018;9:245. Published 2018 Feb 13. doi:10.3389/fimmu.2018.00245.
1664-3224
29497422
10.3389/fimmu.2018.00245
http://hdl.handle.net/10033/622343
Frontiers in immunology
The innate immune system senses influenza A virus (IAV) through different pathogen-recognition receptors including Toll-like receptor 7 (TLR7). Downstream of viral recognition natural killer (NK) cells are activated as part of the anti-IAV immune response. Despite the known decisive role of TLR7 for NK cell activation by therapeutic immunostimulatory RNAs, the contribution of TLR7 to the NK cell response following IAV infection has not been addressed. We have analyzed lung cytokine responses as well as the activation, interferon (IFN)-γ production, and cytotoxicity of lung and splenic NK cells following sublethal respiratory IAV infection in wild-type and TLR7ko mice. Early airway IFN-γ levels as well as the induction of lung NK cell CD69 expression and IFN-γ production in response to IAV infection were significantly attenuated in TLR7-deficient hosts. Strikingly, respiratory IAV infection also primed splenic NK cells for IFN-γ production, degranulation, and target cell lysis, all of which were fully dependent on TLR7. At the same time, lung type I IFN levels were significantly reduced in TLR7ko mice early following IAV infection, displaying a potential upstream mechanism of the attenuated NK cell activation observed. Taken together, our data clearly demonstrate a specific role for TLR7 signaling in local and systemic NK cell activation following respiratory IAV infection despite the presence of redundant innate IAV-recognition pathways.
en
Frontiers
Attribution-NonCommercial-ShareAlike 4.0 International
http://creativecommons.org/licenses/by-nc-sa/4.0/
Toll-like receptor 7
influenza A virus
innate immunity
natural killer cells
pathogen-recognition receptors
respiratory infection
Respiratory Influenza A Virus Infection Triggers Local and Systemic Natural Killer Cell Activation Toll-Like Receptor 7.
Article
Other
9
245
Frontiers in immunology
Switzerland
2020-07-07T11:37:40Z
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oai:repository.helmholtz-hzi.de:10033/622343
2020-07-08 03:31:26.778
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/6226242020-12-08T01:48:09Zcom_10033_620591col_10033_620724
Ogger, Patricia P.
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Silva, Johnatas Dutra
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Aghapour, Mahyar
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Persson, Irma Mahmutovic
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Tulen, Christy
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Jurkowska, Renata
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Ubags, Niki D.
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HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.
2020-11-30T16:07:52Z
2020-11-30T16:07:52Z
2020-09-01
Breathe, 16(3), 1-8. doi:10.1183/20734735.0063-2020.
18106838
10.1183/20734735.0063-2020
http://hdl.handle.net/10033/622624
20734735
Breathe
2-s2.0-85094577229
SCOPUS_ID:85094577229
Every year, the European Respiratory Society (ERS) organises the Lung Science Conference (LSC) in Estoril, Portugal, to discuss basic and translational science. The topic of the LSC 2020 was “Metabolic alterations in lung ageing and disease”. In addition to an outstanding scientific programme, the LSC provides excellent opportunities for career development and inclusion of Early Career Members (ECMs). All scientific and poster sessions are chaired by an ECM who is paired with a senior faculty member to allow ECMs to become acquainted with session chairing. In addition, 40 travel bursaries are made available to abstract authors and all bursary recipients are invited to take part in a mentorship lunch. Moreover, there is a session organised by the Early Career Members Committee (ECMC) dedicated to career development. Here, we describe the scientific highlights of LSC 2020 for those who could not attend. The ERS presents several awards at the LSC and here we will highlight all winners of the LSC 2020 awards. The five highest ranked abstracts from ECMs are presented during the Young investigator session. Patricia Ogger (UK) was presented with the William MacNee Award for the best presentation in this session. Several abstracts were selected for programmed oral presentations and Renata Jurkowska (UK) was presented with the inaugural Geoffrey Laurent Award for the best oral presentation. Moreover, the organisers presented eight Distinguished Poster awards to Anne-Sophie Lamort (Germany), Julia Frankenberg Garcia (UK), Johnatas Silva (UK), Pauline Esteves (France), Claudio Bussi (UK), Elodie Picard (France), Felix Ritzmann (Germany) and Alen Faiz (Australia) for their excellent contributions during the poster session.
European Commission
European Respiratory Society
Attribution-NonCommercial 4.0 International
http://creativecommons.org/licenses/by-nc/4.0/
Early career members at the ers lung science conference 2020: Metabolic alterations in lung ageing and disease
Article
16
3
1
8
Breathe
2020-11-30T16:07:53Z
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oai:repository.helmholtz-hzi.de:10033/622624
2020-12-08 01:48:09.667
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/6226612021-01-06T01:33:40Zcom_10033_620591col_10033_620724
Wu, Qingyu
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Jeron, Andreas
2a74a8f4c70f434de4f2c7e67bb547ab
500
Bruder, Dunja
b5a4f0fe11461388fa1e79487e3fb00e
600
http://orcid.org/0000-0003-3066-189X
Schreiber, Jens
58b8fae24802c28f70cbe1ebb197e227
500
Stegemann-Koniszewski, Sabine
7e63c7675535940588d7cd053873de70
500
HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.
2021-01-05T13:01:26Z
2021-01-05T13:01:26Z
2020-11-27
Microorganisms. 2020 Nov 27;8(12):1878. doi: 10.3390/microorganisms8121878.
2076-2607
33260910
10.3390/microorganisms8121878
http://hdl.handle.net/10033/622661
Microorganisms
Allergic airway inflammation (AAI) involves T helper cell type 2 (Th2) and pro-inflammatory responses to aeroallergens and many predisposing factors remain elusive. Influenza A virus (IAV) is a major human pathogen that causes acute respiratory infections and induces specific immune responses essential for viral clearance and resolution of the infection. Beyond acute infection, IAV has been shown to persistently affect lung homeostasis and respiratory immunity. Here we asked how resolved IAV infection affects subsequently induced AAI. Mice infected with a sublethal dose of IAV were sensitized and challenged in an ovalbumin mediated mouse model for AAI after resolution of the acute viral infection. Histological changes, respiratory leukocytes, cytokines and airway hyperreactivity were analyzed in resolved IAV infection alone and in AAI with and without previous IAV infection. More than five weeks after infection, we detected persistent pneumonia with increased activated CD4+ and CD8+ lymphocytes as well as dendritic cells and MHCII expressing macrophages in the lung. Resolved IAV infection significantly affected subsequently induced AAI on different levels including morphological changes, respiratory leukocytes and lymphocytes as well as the pro-inflammatory cytokine responses, which was clearly diminished. We conclude that IAV has exceptional persisting effects on respiratory immunity with substantial consequences for subsequently induced AAI.
en
MDPI
Attribution 4.0 International
http://creativecommons.org/licenses/by/4.0/
allergic airway inflammation
allergic asthma
influenza A virus
macrophages
pro-inflammatory cytokines
respiratory immune regulation
Resolved Influenza A Virus Infection Has Extended Effects on Lung Homeostasis and Attenuates Allergic Airway Inflammation in a Mouse Model.
Article
8
12
Microorganisms
Switzerland
2021-01-05T13:01:27Z
THUMBNAIL
Wu et al.pdf.jpg
Wu et al.pdf.jpg
Generated Thumbnail
image/jpeg
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https://repository.helmholtz-hzi.de/bitstream/10033/622661/6/Wu%20et%20al.pdf.jpg
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MD5
6
false
Wu_supp.pdf.jpg
Wu_supp.pdf.jpg
Generated Thumbnail
image/jpeg
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https://repository.helmholtz-hzi.de/bitstream/10033/622661/8/Wu_supp.pdf.jpg
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MD5
8
false
TEXT
Wu et al.pdf.txt
Wu et al.pdf.txt
Extracted text
text/plain
83361
https://repository.helmholtz-hzi.de/bitstream/10033/622661/5/Wu%20et%20al.pdf.txt
92f9ee34369af822ff89bbdf0fb02a7d
MD5
5
false
Wu_supp.pdf.txt
Wu_supp.pdf.txt
Extracted text
text/plain
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https://repository.helmholtz-hzi.de/bitstream/10033/622661/7/Wu_supp.pdf.txt
144f6aa75fb98fbf35d08b0738f2dc18
MD5
7
false
LICENSE
license.txt
license.txt
text/plain
1685
https://repository.helmholtz-hzi.de/bitstream/10033/622661/4/license.txt
cb598eeb10bfed09d26fd8d285172ad4
MD5
4
false
CC-LICENSE
license_rdf
license_rdf
application/rdf+xml; charset=utf-8
908
https://repository.helmholtz-hzi.de/bitstream/10033/622661/3/license_rdf
0175ea4a2d4caec4bbcc37e300941108
MD5
3
false
ORIGINAL
Wu et al.pdf
Wu et al.pdf
Open Access publication
application/pdf
4014981
https://repository.helmholtz-hzi.de/bitstream/10033/622661/1/Wu%20et%20al.pdf
762c687036bca726a10a47051b7f5315
MD5
1
true
Wu_supp.pdf
Wu_supp.pdf
supplemental information
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https://repository.helmholtz-hzi.de/bitstream/10033/622661/2/Wu_supp.pdf
d3c0e81e31aea049fe5ba0e7a5fca609
MD5
2
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10033/622661
oai:repository.helmholtz-hzi.de:10033/622661
2021-01-06 01:33:40.244
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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
oai:repository.helmholtz-hzi.de:10033/6227992021-03-27T01:28:57Zcom_10033_311308com_10033_620591col_10033_620724col_10033_620721
Volckmar, Julia
b6205d43b59ee04ade2d9a3fd441ad18
500
Knop, Laura
adefe746852b753f7d5adc631e87a9b2
500
Hirsch, Tatjana
bfe1a842e5ef3cc3fc620dd603498586
500
Frentzel, Sarah
2de1c8e64790256ddc0520207a78c48b
500
Erck, Christian
32ba43e9fc0a6988ac7d08ee4321d877
500
van Ham, Marco
702d5515ad73f4b2c2641e71a6c815a2
500
Stegemann-Koniszewski, Sabine
7e63c7675535940588d7cd053873de70
500
Bruder, Dunja
1ba4133d9ea07fbb30b11e97f4ab5bda
500
HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.
2021-03-26T12:21:46Z
2021-03-26T12:21:46Z
2021-02-05
J Vis Exp. 2021 Feb 5;(168). doi: 10.3791/62018.
33616089
10.3791/62018
http://hdl.handle.net/10033/622799
1940-087X
Journal of visualized experiments : JoVE
Targeted antigen delivery to cross-presenting dendritic cells (DC) in vivo efficiently induces T effector cell responses and displays a valuable approach in vaccine design. Antigen is delivered to DC via antibodies specific for endocytosis receptors such as DEC-205 that induce uptake, processing, and MHC class I- and II-presentation. Efficient and reliable conjugation of the desired antigen to a suitable antibody is a critical step in DC targeting and among other factors depends on the format of the antigen. Chemical conjugation of full-length protein to purified antibodies is one possible strategy. In the past, we have successfully established cross-linking of the model antigen ovalbumin (OVA) and a DEC-205-specific IgG2a antibody (αDEC-205) for in vivo DC targeting studies in mice. The first step of the protocol is the purification of the antibody from the supernatant of the NLDC (non-lymphoid dendritic cells)-145 hybridoma by affinity chromatography. The purified antibody is activated for chemical conjugation by sulfo-SMCC (sulfosuccinimidyl 4-[N-maleimidomethyl] cyclohexane-1-carboxylate) while at the same time the sulfhydryl-groups of the OVA protein are exposed through incubation with TCEP-HCl (tris (2-carboxyethyl) phosphine hydrochloride). Excess TCEP-HCl and sulfo-SMCC are removed and the antigen is mixed with the activated antibody for overnight coupling. The resulting αDEC-205/OVA conjugate is concentrated and freed from unbound OVA. Successful conjugation of OVA to αDEC-205 is verified by western blot analysis and enzyme-linked immunosorbent assay (ELISA). We have successfully used chemically crosslinked αDEC-205/OVA to induce cytotoxic T cell responses in the liver and to compare different adjuvants for their potential in inducing humoral and cellular immunity following in vivo targeting of DEC-205+ DC. Beyond that, such chemically coupled antibody/antigen conjugates offer valuable tools for the efficient induction of vaccine responses to tumor antigens and have been proven to be superior to classical immunization approaches regarding the prevention and therapy of various types of tumors.
en
MyJove Corporation
Attribution-NonCommercial 4.0 International
http://creativecommons.org/licenses/by-nc/4.0/
Chemical Conjugation of a Purified DEC-205-Directed Antibody with Full-Length Protein for Targeting Mouse Dendritic Cells In Vitro and In Vivo.
Article
168
Journal of visualized experiments : JoVE
United States
THUMBNAIL
2021-08-05
Volckmar et al.pdf.jpg
Volckmar et al.pdf.jpg
Generated Thumbnail
image/jpeg
85057
https://repository.helmholtz-hzi.de/bitstream/10033/622799/5/Volckmar%20et%20al.pdf.jpg
e577c69760cc2c7c3c6e2d6a25a4fa07
MD5
5
false
TEXT
2021-08-05
Volckmar et al.pdf.txt
Volckmar et al.pdf.txt
Extracted text
text/plain
51926
https://repository.helmholtz-hzi.de/bitstream/10033/622799/4/Volckmar%20et%20al.pdf.txt
64983c00ffc08956b47b6d0ef984c958
MD5
4
false
LICENSE
license.txt
license.txt
text/plain
1685
https://repository.helmholtz-hzi.de/bitstream/10033/622799/3/license.txt
cb598eeb10bfed09d26fd8d285172ad4
MD5
3
false
CC-LICENSE
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application/rdf+xml; charset=utf-8
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https://repository.helmholtz-hzi.de/bitstream/10033/622799/2/license_rdf
24013099e9e6abb1575dc6ce0855efd5
MD5
2
false
ORIGINAL
Volckmar et al.pdf
Volckmar et al.pdf
accepted manuscript
application/pdf
395796
https://repository.helmholtz-hzi.de/bitstream/10033/622799/1/Volckmar%20et%20al.pdf
02be63efa773115c851bd9b68f6cfd1d
MD5
1
true
10033/622799
oai:repository.helmholtz-hzi.de:10033/622799
2021-03-27 01:28:57.864
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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
oai:repository.helmholtz-hzi.de:10033/6228232021-04-08T01:40:59Zcom_10033_128109com_10033_620659com_10033_620591col_10033_128110col_10033_620724col_10033_620660
Elfaki, Yassin
b7ac992d2de87d19940f2622e92869f0
500
Robert, Philippe A
b943b7622feddf538cc52c707cf425b5
500
Binz, Christoph
f3fc7a6581143e981a0c1b32854ee552
300
Falk, Christine S
84fa0c3390a25e71bc272964dddb40ff
Bruder, Dunja
b5a4f0fe11461388fa1e79487e3fb00e
600
http://orcid.org/0000-0003-3066-189X
Prinz, Immo
4a3aae181793927d1b7907eb1a77b222
500
Floess, Stefan
5ffe089d50f6ea39d568657c60ebcc8f
500
Meyer-Hermann, Michael
f054b81293a071d59f3be787198a3299
Huehn, Jochen
81855dd40035a02edad8ee83ce210282
500
HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.; BRICS, Braunschweiger Zentrum für Systembiologie, Rebenring 56,38106 Braunschweig, Germany.
2021-04-07T14:24:38Z
2021-04-07T14:24:38Z
2021-02-26
Eur J Immunol. 2021 Feb 26. doi: 10.1002/eji.202048981. Epub ahead of print.
33638148
10.1002/eji.202048981
http://hdl.handle.net/10033/622823
1521-4141
European journal of immunology
Foxp3+ Treg cells, which are crucial for maintenance of self-tolerance, mainly develop within the thymus, where they arise from CD25+ Foxp3- or CD25- Foxp3+ Treg cell precursors. Although it is known that infections can cause transient thymic involution, the impact of infection-induced thymus atrophy on thymic Treg (tTreg) cell development is unknown. Here, we infected mice with influenza A virus (IAV) and studied thymocyte population dynamics post infection. IAV infection caused a massive, but transient thymic involution, dominated by a loss of CD4+ CD8+ double-positive (DP) thymocytes, which was accompanied by a significant increase in the frequency of CD25+ Foxp3+ tTreg cells. Differential apoptosis susceptibility could be experimentally excluded as a reason for the relative tTreg cell increase, and mathematical modeling suggested that enhanced tTreg cell generation cannot explain the increased frequency of tTreg cells. Yet, an increased death of DP thymocytes and augmented exit of single-positive (SP) thymocytes was suggested to be causative. Interestingly, IAV-induced thymus atrophy resulted in a significantly reduced T-cell receptor (TCR) repertoire diversity of newly produced tTreg cells. Taken together, IAV-induced thymus atrophy is substantially altering the dynamics of major thymocyte populations, finally resulting in a relative increase of tTreg cells with an altered TCR repertoire.
en
Wiley-VCH
Attribution 4.0 International
http://creativecommons.org/licenses/by/4.0/
Foxp3+ Treg cells ⋅ Influenza A virus ⋅ Mathematical modeling ⋅ Ordinary differential equations ⋅ Thymus atrophy
Influenza A virus-induced thymus atrophy differentially affects dynamics of conventional and regulatory T-cell development in mice.
Article
European journal of immunology
Germany
2021-04-07T14:24:38Z
THUMBNAIL
Elfaki et al.pdf.jpg
Elfaki et al.pdf.jpg
Generated Thumbnail
image/jpeg
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https://repository.helmholtz-hzi.de/bitstream/10033/622823/5/Elfaki%20et%20al.pdf.jpg
d43c44c13944032b496275f2bd03b1e1
MD5
5
false
TEXT
Elfaki et al.pdf.txt
Elfaki et al.pdf.txt
Extracted text
text/plain
81273
https://repository.helmholtz-hzi.de/bitstream/10033/622823/4/Elfaki%20et%20al.pdf.txt
aa0ee7a64544d397e1524bf06898e655
MD5
4
false
LICENSE
license.txt
license.txt
text/plain
1685
https://repository.helmholtz-hzi.de/bitstream/10033/622823/3/license.txt
cb598eeb10bfed09d26fd8d285172ad4
MD5
3
false
CC-LICENSE
license_rdf
license_rdf
application/rdf+xml; charset=utf-8
908
https://repository.helmholtz-hzi.de/bitstream/10033/622823/2/license_rdf
0175ea4a2d4caec4bbcc37e300941108
MD5
2
false
ORIGINAL
Elfaki et al.pdf
Elfaki et al.pdf
Open Access publication
application/pdf
1620632
https://repository.helmholtz-hzi.de/bitstream/10033/622823/1/Elfaki%20et%20al.pdf
b0ff8726d0a952cd7f7a6f43689ebd83
MD5
1
true
10033/622823
oai:repository.helmholtz-hzi.de:10033/622823
2021-04-08 01:40:59.35
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/6228312021-04-20T02:45:37Zcom_10033_620591col_10033_620724
Roth, Stefan
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Li, Ting
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Boehme, Julia D
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Chauhan, Dhruv
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Zhu, Jie
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Ricci, Alessio
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Gorka, Oliver
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Asare, Yaw
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Yang, Jun
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Lopez, Mary S
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Rehberg, Markus
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Bruder, Dunja
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Zhang, Shengxiang
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Groß, Olaf
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Dichgans, Martin
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Hornung, Veit
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Liesz, Arthur
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HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.
2021-04-19T12:18:57Z
2021-04-19T12:18:57Z
2021-03-04
Immunity. 2021 Apr 13;54(4):648-659.e8. doi: 10.1016/j.immuni.2021.02.004. Epub 2021 Mar 4.
33667383
10.1016/j.immuni.2021.02.004
http://hdl.handle.net/10033/622831
1097-4180
Immunity
Loss of lymphocytes, particularly T cell apoptosis, is a central pathological event after severe tissue injury that is associated with increased susceptibility for life-threatening infections. The precise immunological mechanisms leading to T cell death after acute injury are largely unknown. Here, we identified a monocyte-T cell interaction driving bystander cell death of T cells in ischemic stroke and burn injury. Specifically, we found that stroke induced a FasL-expressing monocyte population, which led to extrinsic T cell apoptosis. This phenomenon was driven by AIM2 inflammasome-dependent interleukin-1β (IL-1β) secretion after sensing cell-free DNA. Pharmacological inhibition of this pathway improved T cell survival and reduced post-stroke bacterial infections. As such, this study describes inflammasome-dependent monocyte activation as a previously unstudied cause of T cell death after injury and challenges the current paradigms of post-injury lymphopenia.
en
Elsevier (Cell Press)
Attribution-NonCommercial-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nc-nd/4.0/
AIM2
Fas
IL-1
T cell
burn
cell death
inflammasome
stroke
tissue injury
Post-injury immunosuppression and secondary infections are caused by an AIM2 inflammasome-driven signaling cascade.
Article
54
4
648
659.e8
Immunity
United States
THUMBNAIL
2022-03-04
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2022-03-04
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oai:repository.helmholtz-hzi.de:10033/622831
2021-04-20 02:45:37.457
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/6229712021-08-07T03:28:45Zcom_10033_620591col_10033_620724
Hoang, Quynh Trang Mi
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300
Nguyen, Van Kinh
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Oberacher, Herbert
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Fuchs, Dietmar
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Hernandez-Vargas, Esteban A
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Borucki, Katrin
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Waldburg, Nadine
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Wippermann, Jens
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Schreiber, Jens
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Bruder, Dunja
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http://orcid.org/0000-0003-3066-189X
Veluswamy, Priya
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HZI,Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7,38124 Braunschweig, Germany.
2021-07-29T14:31:42Z
2021-07-29T14:31:42Z
2021-06-08
Front Med (Lausanne). 2021 Jun 8;8:676058. doi: 10.3389/fmed.2021.676058.
2296-858X
34169084
10.3389/fmed.2021.676058
http://hdl.handle.net/10033/622971
Frontiers in medicine
COPD and asthma are two distinct but sometimes overlapping diseases exhibiting varying degrees and types of inflammation on different stages of the disease. Although several biomarkers are defined to estimate the inflammatory endotype and stages in these diseases, there is still a need for new markers and potential therapeutic targets. We investigated the levels of a phytohormone, abscisic acid (ABA) and its receptor, LANCL2, in COPD patients and asthmatics. In addition, PPAR-γ that is activated by ABA in a ligand-binding domain-independent manner was also included in the study. In this study, we correlated ABA with COPD-propagating factors to define the possible role of ABA, in terms of immune regulation, inflammation, and disease stages. We collected blood from 101 COPD patients, 52 asthmatics, and 57 controls. Bronchoscopy was performed on five COPD patients and 29 controls. We employed (i) liquid chromatography-tandem mass spectrometry and HPLC to determine the ABA and indoleamine 2,3-dioxygenase levels, respectively; (ii) real-time PCR to quantify the gene expression of LANCL2 and PPAR-γ; (iii) Flow cytometry to quantify adipocytokines; and (iv) immunoturbidimetry and ELISA to measure CRP and cytokines, respectively. Finally, a multinomial regression model was used to predict the probability of using ABA as a biomarker. Blood ABA levels were significantly reduced in COPD patients and asthmatics compared to age- and gender-matched normal controls. However, PPAR-γ was elevated in COPD patients. Intriguingly, ABA was positively correlated with immune-regulatory factors and was negatively correlated with inflammatory markers, in COPD. Of note, ABA was increased in advanced COPD stages. We thereby conclude that ABA might be involved in regulation of COPD pathogenesis and might be regarded as a potential biomarker for COPD stages.
en
Frontiers
Attribution 4.0 International
http://creativecommons.org/licenses/by/4.0/
COPD
LanCL2
PPAR-γ
abscisic acid
asthma
Serum Concentration of the Phytohormone Abscisic Acid Is Associated With Immune-Regulatory Mediators and Is a Potential Biomarker of Disease Severity in Chronic Obstructive Pulmonary Disease.
Article
8
676058
Frontiers in medicine
Switzerland
2021-07-29T14:31:42Z
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Hoang et al.pdf.txt
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10033/622971
oai:repository.helmholtz-hzi.de:10033/622971
2021-08-07 03:28:45.98
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/6231752022-05-06T01:50:39Zcom_10033_620591col_10033_620724
Aghapour, Mahyar
b555925e886c4a68b6c9c8701c008696
500
Remels, Alexander H V
5aeecb94f77af5614939ab111fa2b8ba
300
Pouwels, Simon D
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300
Bruder, Dunja
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600
http://orcid.org/0000-0003-3066-189X
Hiemstra, Pieter S
93c3910deb26a3f41140261d6564a43b
300
Cloonan, Suzanne M
6798bf3b454690f71c7fd372e8624e9c
300
Heijink, Irene H
78bc0e43ab46203db3c8cc25235defed
300
2022-05-05T13:04:06Z
2022-05-05T13:04:06Z
2019-11-06
2022-05-05
31693390
10.1152/ajplung.00329.2019
http://hdl.handle.net/10033/623175
1522-1504
American journal of physiology. Lung cellular and molecular physiology
Disturbances in mitochondrial structure and function in lung epithelial cells have been implicated in the pathogenesis of various lung diseases, including chronic obstructive pulmonary disease (COPD). Such disturbances affect not only cellular energy metabolism but also alter a range of indispensable cellular homeostatic functions in which mitochondria are known to be involved. These range from cellular differentiation, cell death pathways, and cellular remodeling to physical barrier function and innate immunity, all of which are known to be impacted by exposure to cigarette smoke and have been linked to COPD pathogenesis. Next to their well-established role as the first physical frontline against external insults, lung epithelial cells are immunologically active. Malfunctioning epithelial cells with defective mitochondria are unable to maintain homeostasis and respond adequately to further stress or injury, which may ultimately shape the phenotype of lung diseases. In this review, we provide a comprehensive overview of the impact of cigarette smoke on the development of mitochondrial dysfunction in the lung epithelium and highlight the consequences for cell function, innate immune responses, epithelial remodeling, and epithelial barrier function in COPD. We also discuss the applicability and potential therapeutic value of recently proposed strategies for the restoration of mitochondrial function in the treatment of COPD.
en
Attribution 4.0 International
http://creativecommons.org/licenses/by/4.0/
COPD
cigarette smoke
lung epithelial cells
mitochondrial dysfunction
Mitochondria: at the crossroads of regulating lung epithelial cell function in chronic obstructive pulmonary disease.
Article
318
1
L149
L164
American journal of physiology. Lung cellular and molecular physiology
United States
2022-05-05T13:04:07Z
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10033/623175
oai:repository.helmholtz-hzi.de:10033/623175
2022-05-06 01:50:39.804
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/6232032022-06-14T01:56:10Zcom_10033_620591col_10033_620724
Boehme, Julia D
85e23b3dbea1e741a1320738b1ea31bc
Frentzel, Sarah
2de1c8e64790256ddc0520207a78c48b
500
Bruder, Dunja
1ba4133d9ea07fbb30b11e97f4ab5bda
500
2022-06-13T08:45:09Z
2022-06-13T08:45:09Z
2020-08-03
2020-07-09
32747686
10.1038/s41423-020-0517-5
http://hdl.handle.net/10033/623203
2042-0226
Cellular & molecular immunology
en
Attribution 4.0 International
http://creativecommons.org/licenses/by/4.0/
NMP4: a nuclear driver of innate inflammatory responses during influenza A virus infection.
Article
17
12
1220
1221
Cellular & molecular immunology
China
2022-06-13T08:45:09Z
THUMBNAIL
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MD5
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10033/623203
oai:repository.helmholtz-hzi.de:10033/623203
2022-06-14 01:56:10.903
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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oai:repository.helmholtz-hzi.de:10033/6232142022-06-14T01:56:25Zcom_10033_620591col_10033_620724
Sasaki, Karin
792d9cce9524686394283134463b43cd
300
Bruder, Dunja
b5a4f0fe11461388fa1e79487e3fb00e
600
http://orcid.org/0000-0003-3066-189X
Hernandez-Vargas, Esteban A
f5f76475c898e2d172a51445be77c1ec
2022-06-13T11:09:44Z
2022-06-13T11:09:44Z
2020-02-15
2019-10-07
1007-5704
32288422
10.1016/j.cnsns.2020.105228
http://hdl.handle.net/10033/623214
Communications in nonlinear science & numerical simulation
Co-infections by multiple pathogens have important implications in many aspects of
health, epidemiology and evolution. However, how to disentangle the non-linear dynamics
of the immune response when two infections take place at the same time is largely
unexplored. Using data sets of the immune response during influenza-pneumococcal coinfection
in mice, we employ here topological data analysis to simplify and visualise high
dimensional data sets.
We identified persistent shapes of the simplicial complexes of the data in the three infection
scenarios: single viral infection, single bacterial infection, and co-infection. The
immune response was found to be distinct for each of the infection scenarios and we
uncovered that the immune response during the co-infection has three phases and two
transition points. During the first phase, its dynamics is inherited from its response to
the primary (viral) infection. The immune response has an early shift (few hours post coinfection)
and then modulates its response to react against the secondary (bacterial) infection.
Between 18 and 26 h post co-infection the nature of the immune response changes
again and does no longer resembles either of the single infection scenarios.
en
Attribution-NonCommercial-ShareAlike 4.0 International
http://creativecommons.org/licenses/by-nc-sa/4.0/
Complex data analysis
Immune system dynamics
Influenza infections
Topological data analysis
Topological data analysis to model the shape of immune responses during co-infections.
Article
85
105228
Communications in nonlinear science & numerical simulation
China
2022-06-13T11:09:45Z
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oai:repository.helmholtz-hzi.de:10033/623214
2022-06-14 01:56:25.431
Helmholtz Zentrum für Infektionsforschung Repository
hzi@openrepository.com
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