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Article ; Online: Intraepithelial Lymphocytes of the Intestine.

Lockhart, Ainsley / Mucida, Daniel / Bilate, Angelina M

2024

Abstract: The intestinal epithelium, which segregates the highly stimulatory lumen from the underlying tissue, harbors one of the largest lymphocyte populations in the body, intestinal intraepithelial lymphocytes (IELs). IELs must balance tolerance, resistance, ... ...

Abstract	The intestinal epithelium, which segregates the highly stimulatory lumen from the underlying tissue, harbors one of the largest lymphocyte populations in the body, intestinal intraepithelial lymphocytes (IELs). IELs must balance tolerance, resistance, and tissue protection to maintain epithelial homeostasis and barrier integrity. This review discusses the ontogeny, environmental imprinting, T cell receptor (TCR) repertoire, and function of intestinal IELs. Despite distinct developmental pathways, IEL subsets share core traits including an epithelium-adapted profile, innate-like properties, cytotoxic potential, and limited TCR diversity. IELs also receive important developmental and functional cues through interactions with epithelial cells, microbiota, and dietary components. The restricted TCR diversity of IELs suggests that a limited set of intestinal antigens drives IEL responses, with potential functional consequences. Finally, IELs play a key role in promoting homeostatic immunity and epithelial barrier integrity but can become pathogenic upon dysregulation. Therefore, IELs represent intriguing but underexamined therapeutic targets for inflammatory diseases and cancer. Expected final online publication date for the
Language	English
Publishing date	2024-01-26
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	604953-9
ISSN	1545-3278 ; 0732-0582
ISSN (online)	1545-3278
ISSN	0732-0582
DOI	10.1146/annurev-immunol-090222-100246
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Article ; Online: Stepwise chromatin and transcriptional acquisition of an intraepithelial lymphocyte program.

London, Mariya / Bilate, Angelina M / Castro, Tiago B R / Sujino, Tomohisa / Mucida, Daniel

Nature immunology

2021 Volume 22, Issue 4, Page(s) 449–459

Abstract: Mesenteric lymph node (mLN) T cells undergo tissue adaptation upon migrating to intestinal lamina propria and epithelium, ensuring appropriate balance between tolerance and resistance. By combining mouse genetics with single-cell and chromatin analyses, ... ...

Abstract	Mesenteric lymph node (mLN) T cells undergo tissue adaptation upon migrating to intestinal lamina propria and epithelium, ensuring appropriate balance between tolerance and resistance. By combining mouse genetics with single-cell and chromatin analyses, we uncovered the molecular imprinting of gut epithelium on T cells. Transcriptionally, conventional and regulatory (T
MeSH term(s)	Animals ; Cell Differentiation ; Cell Lineage ; Cells, Cultured ; Chromatin Assembly and Disassembly ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genomic Imprinting ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Intraepithelial Lymphocytes/immunology ; Intraepithelial Lymphocytes/metabolism ; Lymph Nodes/immunology ; Lymph Nodes/metabolism ; Mice, Knockout ; Phenotype ; RNA-Seq ; Single-Cell Analysis ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic ; Transcriptome ; Mice
Chemical Substances	Th-POK protein, mouse ; Transcription Factors
Language	English
Publishing date	2021-03-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-021-00883-8
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 42: Show issues

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Article: Universal recording of cell-cell contacts

Nakandakari-Higa, Sandra / Canesso, Maria C C / Walker, Sarah / Chudnovskiy, Aleksey / Jacobsen, Johanne T / Bilanovic, Jana / Parigi, S Martina / Fiedorczuk, Karol / Fuchs, Elaine / Bilate, Angelina M / Pasqual, Giulia / Mucida, Daniel / Pritykin, Yuri / Victora, Gabriel D

bioRxiv : the preprint server for biology

2023

Abstract: Cellular interactions are essential for tissue organization and functionality. In particular, immune cells rely on direct and usually transient interactions with other immune and non-immune populations to specify and regulate their function. To study ... ...

Abstract	Cellular interactions are essential for tissue organization and functionality. In particular, immune cells rely on direct and usually transient interactions with other immune and non-immune populations to specify and regulate their function. To study these "kiss-and-run" interactions directly
Language	English
Publishing date	2023-04-18
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.03.16.533003
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Article ; Online: Universal recording of immune cell interactions in vivo.

Nakandakari-Higa, Sandra / Walker, Sarah / Canesso, Maria C C / van der Heide, Verena / Chudnovskiy, Aleksey / Kim, Dong-Yoon / Jacobsen, Johanne T / Parsa, Roham / Bilanovic, Jana / Parigi, S Martina / Fiedorczuk, Karol / Fuchs, Elaine / Bilate, Angelina M / Pasqual, Giulia / Mucida, Daniel / Kamphorst, Alice O / Pritykin, Yuri / Victora, Gabriel D

Nature

2024 Volume 627, Issue 8003, Page(s) 399–406

Abstract: Immune cells rely on transient physical interactions with other immune and non-immune populations to regulate their ... ...

Abstract	Immune cells rely on transient physical interactions with other immune and non-immune populations to regulate their function
MeSH term(s)	CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; Cell Communication/immunology ; Dendritic Cells/cytology ; Dendritic Cells/immunology ; Ligands ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; T Follicular Helper Cells/cytology ; T Follicular Helper Cells/immunology ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; Germinal Center/cytology ; Single-Cell Gene Expression Analysis ; Epithelial Cells/cytology ; Epithelial Cells/immunology ; Intestinal Mucosa/cytology ; Intestinal Mucosa/immunology ; Lymphocytic choriomeningitis virus/immunology ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic Choriomeningitis/virology ; Organ Specificity
Chemical Substances	Ligands
Language	English
Publishing date	2024-03-06
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-024-07134-4
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Zs.A 26: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Zs.MO 244: Show issues

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Article ; Online: Induced CD4+Foxp3+ regulatory T cells in immune tolerance.

Bilate, Angelina M / Lafaille, Juan J

Annual review of immunology

2012 Volume 30, Page(s) 733–758

Abstract: Regulatory T lymphocytes are essential to maintain homeostasis of the immune system, limiting the magnitude of effector responses and allowing the establishment of immunological tolerance. Two main types of regulatory T cells have been identified-- ... ...

Abstract	Regulatory T lymphocytes are essential to maintain homeostasis of the immune system, limiting the magnitude of effector responses and allowing the establishment of immunological tolerance. Two main types of regulatory T cells have been identified--natural and induced (or adaptive)-and both play significant roles in tuning down effector immune responses. Adaptive CD4(+)Foxp3(+) regulatory T (iTreg) cells develop outside the thymus under a variety of conditions. These include not only antigen presentation under subimmunogenic or noninflammatory conditions, but also chronic inflammation and infections. We speculate that the different origin of iTreg cells (noninflammatory versus inflammatory) results in distinct properties, including their stability. iTreg cells are also generated during homeostasis of the gut and in cancer, although some cancers also favor expansion of natural regulatory T (nTreg) cells. Here we review how iTreg cells develop and how they participate in immunological tolerance, contrasting, when possible, iTreg cells with nTreg cells.
MeSH term(s)	Adoptive Transfer ; Animals ; Antigen-Presenting Cells/immunology ; Antigen-Presenting Cells/metabolism ; CD4 Antigens/metabolism ; Forkhead Transcription Factors/metabolism ; Humans ; Immune Tolerance/immunology ; Lymphoid Tissue/immunology ; Lymphoid Tissue/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
Chemical Substances	CD4 Antigens ; FOXP3 protein, human ; Forkhead Transcription Factors
Language	English
Publishing date	2012
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604953-9
ISSN	1545-3278 ; 0732-0582
ISSN (online)	1545-3278
ISSN	0732-0582
DOI	10.1146/annurev-immunol-020711-075043
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Microbiota imbalance induced by dietary sugar disrupts immune-mediated protection from metabolic syndrome.

Kawano, Yoshinaga / Edwards, Madeline / Huang, Yiming / Bilate, Angelina M / Araujo, Leandro P / Tanoue, Takeshi / Atarashi, Koji / Ladinsky, Mark S / Reiner, Steven L / Wang, Harris H / Mucida, Daniel / Honda, Kenya / Ivanov, Ivaylo I

Cell

2022 Volume 185, Issue 19, Page(s) 3501–3519.e20

Abstract: How intestinal microbes regulate metabolic syndrome is incompletely understood. We show that intestinal microbiota protects against development of obesity, metabolic syndrome, and pre-diabetic phenotypes by inducing commensal-specific Th17 cells. High- ... ...

Abstract	How intestinal microbes regulate metabolic syndrome is incompletely understood. We show that intestinal microbiota protects against development of obesity, metabolic syndrome, and pre-diabetic phenotypes by inducing commensal-specific Th17 cells. High-fat, high-sugar diet promoted metabolic disease by depleting Th17-inducing microbes, and recovery of commensal Th17 cells restored protection. Microbiota-induced Th17 cells afforded protection by regulating lipid absorption across intestinal epithelium in an IL-17-dependent manner. Diet-induced loss of protective Th17 cells was mediated by the presence of sugar. Eliminating sugar from high-fat diets protected mice from obesity and metabolic syndrome in a manner dependent on commensal-specific Th17 cells. Sugar and ILC3 promoted outgrowth of Faecalibaculum rodentium that displaced Th17-inducing microbiota. These results define dietary and microbiota factors posing risk for metabolic syndrome. They also define a microbiota-dependent mechanism for immuno-pathogenicity of dietary sugar and highlight an elaborate interaction between diet, microbiota, and intestinal immunity in regulation of metabolic disorders.
MeSH term(s)	Animals ; Diet, High-Fat ; Dietary Sugars ; Interleukin-17 ; Intestinal Mucosa ; Lipids ; Metabolic Syndrome ; Mice ; Mice, Inbred C57BL ; Microbiota ; Obesity ; Th17 Cells
Chemical Substances	Dietary Sugars ; Interleukin-17 ; Lipids
Language	English
Publishing date	2022-08-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2022.08.005
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 58: Show issues

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Article: Microbiota imbalance induced by dietary sugar disrupts immune-mediated protection from metabolic syndrome

Kawano, Yoshinaga / Edwards, Madeline / Huang, Yiming / Bilate, Angelina M. / Araujo, Leandro P. / Tanoue, Takeshi / Atarashi, Koji / Ladinsky, Mark S. / Reiner, Steven L. / Wang, Harris H. / Mucida, Daniel / Honda, Kenya / Ivanov, Ivaylo I.

Cell. 2022 Aug. 04,

2022

Abstract	How intestinal microbes regulate metabolic syndrome is incompletely understood. We show that intestinal microbiota protects against development of obesity, metabolic syndrome, and pre-diabetic phenotypes by inducing commensal-specific Th17 cells. High-fat, high-sugar diet promoted metabolic disease by depleting Th17-inducing microbes, and recovery of commensal Th17 cells restored protection. Microbiota-induced Th17 cells afforded protection by regulating lipid absorption across intestinal epithelium in an IL-17-dependent manner. Diet-induced loss of protective Th17 cells was mediated by the presence of sugar. Eliminating sugar from high-fat diets protected mice from obesity and metabolic syndrome in a manner dependent on commensal-specific Th17 cells. Sugar and ILC3 promoted outgrowth of Faecalibaculum rodentium that displaced Th17-inducing microbiota. These results define dietary and microbiota factors posing risk for metabolic syndrome. They also define a microbiota-dependent mechanism for immuno-pathogenicity of dietary sugar and highlight an elaborate interaction between diet, microbiota, and intestinal immunity in regulation of metabolic disorders.
Keywords	absorption ; high carbohydrate diet ; immunity ; intestinal microorganisms ; intestinal mucosa ; lipids ; metabolic diseases ; metabolic syndrome ; obesity ; risk ; sugars
Language	English
Dates of publication	2022-0804
Publishing place	Elsevier Inc.
Document type	Article
Note	Pre-press version
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2022.08.005
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: T Cell Receptor Is Required for Differentiation, but Not Maintenance, of Intestinal CD4

Bilate, Angelina M / London, Mariya / Castro, Tiago B R / Mesin, Luka / Bortolatto, Juliana / Kongthong, Suppawat / Harnagel, Audrey / Victora, Gabriel D / Mucida, Daniel

Immunity

2020 Volume 53, Issue 5, Page(s) 1001–1014.e20

Abstract: The gut epithelium is populated by intraepithelial lymphocytes (IELs), a heterogeneous T cell population with cytotoxic and regulatory properties, which can be acquired at the epithelial layer. However, the role of T cell receptor (TCR) in this process ... ...

Abstract	The gut epithelium is populated by intraepithelial lymphocytes (IELs), a heterogeneous T cell population with cytotoxic and regulatory properties, which can be acquired at the epithelial layer. However, the role of T cell receptor (TCR) in this process remains unclear. Single-cell transcriptomic analyses revealed distinct clonal expansions between cell states, with CD4
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Clonal Evolution/genetics ; Clonal Evolution/immunology ; Histocompatibility Antigens Class II/genetics ; Histocompatibility Antigens Class II/immunology ; Immunophenotyping ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Intraepithelial Lymphocytes/immunology ; Intraepithelial Lymphocytes/metabolism ; Mice ; Receptors, Antigen, T-Cell/metabolism ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Signal Transduction ; Single-Cell Analysis ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism
Chemical Substances	Histocompatibility Antigens Class II ; Receptors, Antigen, T-Cell ; Receptors, Antigen, T-Cell, alpha-beta
Language	English
Publishing date	2020-10-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2020.09.003
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 69: Show issues

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Article ; Online: Can TNF-α boost regulatory T cells?

Bilate, Angelina M / Lafaille, Juan J

The Journal of clinical investigation

2010 Volume 120, Issue 12, Page(s) 4190–4192

Abstract: Deleterious immune responses that cause autoimmune diseases such as type 1 diabetes are normally kept in check by a myriad of mechanisms. Among these, protection mediated by CD4+Foxp3+ Tregs constitutes an essential pathway. Much work over the past ... ...

Abstract	Deleterious immune responses that cause autoimmune diseases such as type 1 diabetes are normally kept in check by a myriad of mechanisms. Among these, protection mediated by CD4+Foxp3+ Tregs constitutes an essential pathway. Much work over the past decade aimed to understand how Tregs affect immune responses triggered by effector T cells (Teffs), but less is known about how Teffs affect Tregs. In this issue of the JCI, Grinberg-Bleyer et al. report the clearest example thus far regarding this important aspect of Treg biology. They find that in mice, sustained protection from diabetes by Tregs is dependent on Teffs and partially dependent on TNF-α, a cytokine traditionally considered proinflammatory.
MeSH term(s)	Animals ; Diabetes Mellitus, Type 1/immunology ; Feedback, Physiological ; Lymphocyte Cooperation ; Mice ; Models, Immunological ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/immunology ; Tumor Necrosis Factor-alpha/immunology
Chemical Substances	Tumor Necrosis Factor-alpha
Language	English
Publishing date	2010-11-22
Publishing country	United States
Document type	Comment ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI45262
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Article ; Online: A minimally-edited mouse model for infection with multiple SARS-CoV-2 strains.

Nakandakari-Higa, Sandra / Parsa, Roham / Reis, Bernardo S / de Carvalho, Renan V H / Mesin, Luka / Hoffmann, Hans-Heinrich / Bortolatto, Juliana / Muramatsu, Hiromi / Lin, Paulo J C / Bilate, Angelina M / Rice, Charles M / Pardi, Norbert / Mucida, Daniel / Victora, Gabriel D / Canesso, Maria Cecilia C

Frontiers in immunology

2022 Volume 13, Page(s) 1007080

Abstract: Efficient mouse models to study SARS-CoV-2 infection are critical for the development and assessment of vaccines and therapeutic approaches to mitigate the current pandemic and prevent reemergence of COVID-19. While the first generation of mouse models ... ...

Abstract	Efficient mouse models to study SARS-CoV-2 infection are critical for the development and assessment of vaccines and therapeutic approaches to mitigate the current pandemic and prevent reemergence of COVID-19. While the first generation of mouse models allowed SARS-CoV-2 infection and pathogenesis, they relied on ectopic expression and non-physiological levels of human angiotensin-converting enzyme 2 (hACE2). Here we generated a mouse model carrying the minimal set of modifications necessary for productive infection with multiple strains of SARS-CoV-2. Substitution of only three amino acids in the otherwise native mouse
MeSH term(s)	Humans ; Mice ; Animals ; SARS-CoV-2 ; Angiotensin-Converting Enzyme 2/genetics ; COVID-19 ; Disease Models, Animal ; Pandemics
Chemical Substances	Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2022-11-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1007080
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