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Article ; Online: Gingival fibroblast activation by Porphyromonas gingivalis is driven by TLR2 and is independent of the LPS-TLR4 axis.

Schuster, Aureliusz / Nieboga, Elwira / Kantorowicz, Malgorzata / Lipska, Weronika / Kaczmarzyk, Tomasz / Potempa, Jan / Grabiec, Aleksander M

European journal of immunology

2024 Volume 54, Issue 3, Page(s) e2350776

Abstract: Gingival fibroblasts (GFs) are abundant structural cells of the periodontium that contribute to the host's innate immunity by producing cytokines and chemokines in response to oral pathogens, such as Porphyromonas gingivalis. Isolated lipopolysaccharide ( ...

Abstract	Gingival fibroblasts (GFs) are abundant structural cells of the periodontium that contribute to the host's innate immunity by producing cytokines and chemokines in response to oral pathogens, such as Porphyromonas gingivalis. Isolated lipopolysaccharide (Pg-LPS) is commonly used to study GF responses to P. gingivalis; however, this approach produced conflicting observations regarding its proinflammatory potential and the engagement of specific Toll-like receptors (TLRs). In this work, we demonstrate that commercially available Pg-LPS preparations are weak activators of GF innate immune responses compared with live P. gingivalis or other relevant virulence factors, such as P. gingivalis fimbriae or LPS from Escherichia coli. GF's nonresponsiveness to Pg-LPS can be only partly attributed to the low expression of TLR4 and its accessory molecules, CD14 and LY36, and is likely caused by the unique structure and composition of the Pg-LPS lipid A. Finally, we combined gene silencing and neutralizing antibody studies to demonstrate that GF response to infection with live P. gingivalis relies predominantly on TLR2. In contrast, the LPS-TLR4 signaling plays a negligible role in inflammatory cytokine production by GFs exposed to this oral pathogen, confirming that Pg-LPS stimulation is not an optimal model for studies of GF responses to P. gingivalis.
MeSH term(s)	Lipopolysaccharides ; Porphyromonas gingivalis ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 2/metabolism ; Toll-Like Receptor 4/metabolism ; Fibroblasts
Chemical Substances	Lipopolysaccharides ; Toll-Like Receptor 2 ; Toll-Like Receptor 4
Language	English
Publishing date	2024-01-08
Publishing country	Germany
Document type	Journal Article
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.202350776
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Article ; Online: Identification of a new genetic variant (G231N, E232T, N235D) of peptidylarginine deiminase from

Bereta, Grzegorz P / Strzelec, Karolina / Łazarz-Bartyzel, Katarzyna / Dziedzic-Kowalska, Agata / Nowakowska, Zuzanna / Krutyhołowa, Anna / Bielecka, Ewa / Kantyka, Tomasz / Grabiec, Aleksander M / Kaczmarzyk, Tomasz / Chomyszyn-Gajewska, Maria / Potempa, Jan / Gawron, Katarzyna

Frontiers in immunology

2024 Volume 15, Page(s) 1355357

Abstract: Chronic periodontitis (CP), an inflammatory disease of periodontal tissues driven by a dysbiotic subgingival bacterial biofilm, is also associated with several systemic diseases, including rheumatoid arthritis (RA). ...

Abstract	Chronic periodontitis (CP), an inflammatory disease of periodontal tissues driven by a dysbiotic subgingival bacterial biofilm, is also associated with several systemic diseases, including rheumatoid arthritis (RA).
MeSH term(s)	Humans ; Protein-Arginine Deiminases/genetics ; Protein-Arginine Deiminases/metabolism ; Porphyromonas gingivalis ; Peptides ; Periodontium/metabolism ; Chronic Periodontitis/genetics
Chemical Substances	Protein-Arginine Deiminases (EC 3.5.3.15) ; Peptides
Language	English
Publishing date	2024-03-21
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.2024.1355357
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Article ; Online: Epigenetic regulation of inflammation in periodontitis: cellular mechanisms and therapeutic potential.

Jurdziński, Krzysztof T / Potempa, Jan / Grabiec, Aleksander M

Clinical epigenetics

2020 Volume 12, Issue 1, Page(s) 186

Abstract: Epigenetic mechanisms, namely DNA and histone modifications, are critical regulators of immunity and inflammation which have emerged as potential targets for immunomodulating therapies. The prevalence and significant morbidity of periodontitis, in ... ...

Abstract	Epigenetic mechanisms, namely DNA and histone modifications, are critical regulators of immunity and inflammation which have emerged as potential targets for immunomodulating therapies. The prevalence and significant morbidity of periodontitis, in combination with accumulating evidence that genetic, environmental and lifestyle factors cannot fully explain the susceptibility of individuals to disease development, have driven interest in epigenetic regulation as an important factor in periodontitis pathogenesis. Aberrant promoter methylation profiles of genes involved in inflammatory activation, including TLR2, PTGS2, IFNG, IL6, IL8, and TNF, have been observed in the gingival tissue, peripheral blood or buccal mucosa from patients with periodontitis, correlating with changes in expression and disease severity. The expression of enzymes that regulate histone acetylation, in particular histone deacetylases (HDACs), is also dysregulated in periodontitis-affected gingival tissue. Infection of gingival epithelial cells, gingival fibroblasts and periodontal ligament cells with the oral pathogens Porphyromonas gingivalis or Treponema denticola induces alterations in expression and activity of chromatin-modifying enzymes, as well as site-specific and global changes in DNA methylation profiles and in histone acetylation and methylation marks. These epigenetic changes are associated with excessive production of inflammatory cytokines, chemokines, and matrix-degrading enzymes that can be suppressed by small molecule inhibitors of HDACs (HDACi) or DNA methyltransferases. HDACi and inhibitors of bromodomain-containing BET proteins ameliorate inflammation, osteoclastogenesis, and alveolar bone resorption in animal models of periodontitis, suggesting their clinical potential as host modulation therapeutic agents. However, broader application of epigenomic methods will be required to create a comprehensive map of epigenetic changes in periodontitis. The integration of functional studies with global analyses of the epigenetic landscape will provide critical information on the therapeutic and diagnostic potential of epigenetics in periodontal disease.
MeSH term(s)	Animals ; Case-Control Studies ; CpG Islands ; Cytokines/metabolism ; DNA Methylation ; Epigenomics/methods ; Epithelial Cells/metabolism ; Epithelial Cells/microbiology ; Fibroblasts/metabolism ; Histone Code/genetics ; Histone Deacetylases/genetics ; Humans ; Inflammation/genetics ; Mice ; Models, Animal ; Periodontitis/epidemiology ; Periodontitis/genetics ; Periodontitis/pathology ; Periodontitis/therapy ; Porphyromonas gingivalis/genetics ; Porphyromonas gingivalis/isolation & purification ; Prevalence ; Promoter Regions, Genetic/genetics ; Proteins/antagonists & inhibitors ; Proteins/metabolism ; Rats ; Severity of Illness Index ; Treponema denticola/genetics ; Treponema denticola/isolation & purification
Chemical Substances	Cytokines ; Proteins ; bromodomain and extra-terminal domain protein, human ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2020-11-30
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2553921-8
ISSN	1868-7083 ; 1868-7075
ISSN (online)	1868-7083
ISSN	1868-7075
DOI	10.1186/s13148-020-00982-7
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Article ; Online: Accessory fimbrial subunits and PPAD are necessary for TLR2 activation by Porphyromonas gingivalis.

Wielento, Aleksandra / Bereta, Grzegorz P / Szczęśniak, Katarzyna / Jacuła, Anna / Terekhova, Marina / Artyomov, Maxim N / Hasegawa, Yoshiaki / Grabiec, Aleksander M / Potempa, Jan

Molecular oral microbiology

2023 Volume 38, Issue 4, Page(s) 334–346

Abstract: Porphyromonas gingivalis is an oral pathogen that promotes dysbiosis by quenching the bactericidal activity of the host immune system while maintaining chronic inflammation, leading to periodontitis. This involves the secretion of virulence factors such ... ...

Abstract	Porphyromonas gingivalis is an oral pathogen that promotes dysbiosis by quenching the bactericidal activity of the host immune system while maintaining chronic inflammation, leading to periodontitis. This involves the secretion of virulence factors such as P. gingivalis peptidyl arginine deiminase (PPAD), which converts the C-terminal Arg residues of bacterial and host-derived proteins and peptides into citrulline. We have previously shown that PPAD activity and major fimbriae (containing FimA) are necessary for P. gingivalis to activate Toll-like receptor 2 (TLR2). TLR2 is an important component of the innate immune system and plays a predominant role in the recognition of P. gingivalis by host cells. Here, we extend those findings to show that P. gingivalis strains deficient for PPAD and fimbriae induced almost identical transcriptional profiles in infected primary human gingival fibroblasts (PHGFs), but these differed substantially from the transcriptome elicited by the wild-type ATCC 33277 strain. Apparently, PPAD-modified fimbriae trigger the host cell response to P. gingivalis, as confirmed by showing that the proinflammatory host cell response mediated by TLR2 is dependent on PPAD activity and the presence of fimbriae, with type I fimbriae as the most potent TLR2 activators. We also found that PPAD-modified accessory fimbrial subunits (FimC, FimD, and FimE) alone or in combination are TLR2 ligands in a reporter cell line. Although FimA polymerization to form the fimbrial shaft was not required for TLR2 activation, the secretion and proteolytic maturation of FimA were necessary for signaling by accessory Fim proteins. This was supported by showing that the proinflammatory activation of PHGFs is dependent on PPAD and accessory fimbrial subunits. We conclude that accessory fimbrial subunits are modified by PPAD and stimulate the response to P. gingivalis infection in a TLR2-dependent manner.
MeSH term(s)	Humans ; Protein-Arginine Deiminases/metabolism ; Porphyromonas gingivalis ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 2/metabolism ; Fimbriae, Bacterial/metabolism ; Gingiva/microbiology
Chemical Substances	Protein-Arginine Deiminases (EC 3.5.3.15) ; Toll-Like Receptor 2 ; TLR2 protein, human
Language	English
Publishing date	2023-06-22
Publishing country	Denmark
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2537726-7
ISSN	2041-1014 ; 2041-1006
ISSN (online)	2041-1014
ISSN	2041-1006
DOI	10.1111/omi.12427
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Zs.A 2199: Show issues

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Article ; Online: TLR2 Activation by

Wielento, Aleksandra / Bereta, Grzegorz P / Łagosz-Ćwik, Katarzyna B / Eick, Sigrun / Lamont, Richard J / Grabiec, Aleksander M / Potempa, Jan

Frontiers in immunology

2022 Volume 13, Page(s) 823685

Abstract: Porphyromonas ... ...

Abstract	Porphyromonas gingivalis
MeSH term(s)	Dinoprostone/metabolism ; Humans ; Periodontitis/metabolism ; Porphyromonas gingivalis ; Protein-Arginine Deiminases/metabolism ; Toll-Like Receptor 2/metabolism
Chemical Substances	TLR2 protein, human ; Toll-Like Receptor 2 ; Protein-Arginine Deiminases (EC 3.5.3.15) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2022-04-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.823685
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Article: Epigenetic regulation in bacterial infections: targeting histone deacetylases

Grabiec, Aleksander M / Potempa, Jan

Critical reviews in microbiology. 2018 May 4, v. 44, no. 3

2018

Abstract: Pathogens have developed sophisticated strategies to evade the immune response, among which manipulation of host cellular epigenetic mechanisms plays a prominent role. In the last decade, modulation of histone acetylation in host cells has emerged as an ... ...

Abstract	Pathogens have developed sophisticated strategies to evade the immune response, among which manipulation of host cellular epigenetic mechanisms plays a prominent role. In the last decade, modulation of histone acetylation in host cells has emerged as an efficient strategy of bacterial immune evasion. Virulence factors and metabolic products of pathogenic microorganisms alter expression and activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs) to suppress transcription of host defense genes through epigenetic changes in histone acetylation marks. This new avenue of pathogen–host interactions is particularly important in light of introduction of HDAC inhibitors into clinical practice. Considerable effort is currently being applied to better understand the effects of HDAC inhibitors on the quality of immune responses to pathogens and to characterize the therapeutic potential of these compounds in microbial infections. In this review, we will discuss the recently discovered mechanisms utilized by bacteria to facilitate their survival within infected hosts through subversion of the host acetylation system and the effects of acetylation modulators, including HDAC inhibitors and bromodomain-containing BET protein inhibitors, on innate immune responses against microbial pathogens. Integration of these two lines of experimental evidence provides critical information on the perspectives of epigenetic therapies targeting protein acetylation in infectious diseases.
Keywords	acetylation ; acetyltransferases ; bacteria ; bacterial infections ; epigenetics ; genes ; histone deacetylase ; histones ; host-pathogen relationships ; hosts ; immune evasion ; immune response ; innate immunity ; pathogens ; therapeutics ; transcription (genetics) ; virulence
Language	English
Dates of publication	2018-0504
Size	p. 336-350.
Publishing place	Taylor & Francis
Document type	Article
ZDB-ID	1053620-6
ISSN	1549-7828 ; 1040-841X
ISSN (online)	1549-7828
ISSN	1040-841X
DOI	10.1080/1040841X.2017.1373063
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Epigenetic regulation in bacterial infections: targeting histone deacetylases.

Grabiec, Aleksander M / Potempa, Jan

Critical reviews in microbiology

2017 Volume 44, Issue 3, Page(s) 336–350

Abstract	Pathogens have developed sophisticated strategies to evade the immune response, among which manipulation of host cellular epigenetic mechanisms plays a prominent role. In the last decade, modulation of histone acetylation in host cells has emerged as an efficient strategy of bacterial immune evasion. Virulence factors and metabolic products of pathogenic microorganisms alter expression and activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs) to suppress transcription of host defense genes through epigenetic changes in histone acetylation marks. This new avenue of pathogen-host interactions is particularly important in light of introduction of HDAC inhibitors into clinical practice. Considerable effort is currently being applied to better understand the effects of HDAC inhibitors on the quality of immune responses to pathogens and to characterize the therapeutic potential of these compounds in microbial infections. In this review, we will discuss the recently discovered mechanisms utilized by bacteria to facilitate their survival within infected hosts through subversion of the host acetylation system and the effects of acetylation modulators, including HDAC inhibitors and bromodomain-containing BET protein inhibitors, on innate immune responses against microbial pathogens. Integration of these two lines of experimental evidence provides critical information on the perspectives of epigenetic therapies targeting protein acetylation in infectious diseases.
MeSH term(s)	Animals ; Bacteria/genetics ; Bacteria/metabolism ; Bacterial Infections/enzymology ; Bacterial Infections/genetics ; Bacterial Infections/metabolism ; Bacterial Infections/microbiology ; Epigenesis, Genetic ; Histone Deacetylase Inhibitors/metabolism ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Host-Pathogen Interactions ; Humans
Chemical Substances	Histone Deacetylase Inhibitors ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2017-10-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1053620-6
ISSN	1549-7828 ; 1040-841X
ISSN (online)	1549-7828
ISSN	1040-841X
DOI	10.1080/1040841X.2017.1373063
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Article ; Online: Immunopathology of lung diseases: introduction for the special issue.

Hussell, Tracy / Grabiec, Aleksander M

Seminars in immunopathology

2016 Volume 38, Issue 4, Page(s) 407–408

MeSH term(s)	Animals ; Cytokines/immunology ; Dendritic Cells/immunology ; Dendritic Cells/pathology ; Humans ; Immunity, Innate ; Killer Cells, Natural/immunology ; Killer Cells, Natural/pathology ; Lung Diseases/immunology ; Lung Diseases/pathology ; Lymphocytes/immunology ; Lymphocytes/pathology ; Macrophages/metabolism ; Macrophages/pathology
Chemical Substances	Cytokines
Keywords	covid19
Language	English
Publishing date	2016-05-19
Publishing country	Germany
Document type	Editorial
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-016-0572-2
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Article ; Online: The role of airway macrophages in apoptotic cell clearance following acute and chronic lung inflammation.

Grabiec, Aleksander M / Hussell, Tracy

Seminars in immunopathology

2016 Volume 38, Issue 4, Page(s) 409–423

Abstract: Acute and chronic inflammatory responses in the lung are associated with the accumulation of large quantities of immune and structural cells undergoing apoptosis, which need to be engulfed by phagocytes in a process called 'efferocytosis'. Apoptotic cell ...

Abstract	Acute and chronic inflammatory responses in the lung are associated with the accumulation of large quantities of immune and structural cells undergoing apoptosis, which need to be engulfed by phagocytes in a process called 'efferocytosis'. Apoptotic cell recognition and removal from the lung is mediated predominantly by airway macrophages, though immature dendritic cells and non-professional phagocytes, such as epithelial cells and mesenchymal cells, can also display this function. Efficient clearance of apoptotic cells from the airways is essential for successful resolution of inflammation and the return to lung homeostasis. Disruption of this process leads to secondary necrosis of accumulating apoptotic cells, release of necrotic cell debris and subsequent uncontrolled inflammatory activation of the innate immune system by the released 'damage associated molecular patterns' (DAMPS). To control the duration of the immune response and prevent autoimmune reactions, anti-inflammatory signalling cascades are initiated in the phagocyte upon apoptotic cell uptake, mediated by a range of receptors that recognise specific phospholipids or proteins externalised on, or secreted by, the apoptotic cell. However, prolonged activation of apoptotic cell recognition receptors, such as the family of receptor tyrosine kinases Tyro3, Axl and MerTK (TAM), may delay or prevent inflammatory responses to subsequent infections. In this review, we will discuss recent advances in our understanding of the mechanism controlling apoptotic cell recognition and removal from the lung in homeostasis and during inflammation, the contribution of defective efferocytosis to chronic inflammatory lung diseases, such as chronic obstructive pulmonary disease, asthma and cystic fibrosis, and implications of the signals triggered by apoptotic cells in the susceptibility to pulmonary microbial infections.
MeSH term(s)	Acute Disease ; Animals ; Apoptosis/immunology ; Biomarkers ; Cell Communication/immunology ; Chronic Disease ; Humans ; Immunity ; Inflammation/etiology ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/pathology ; Lung Diseases/etiology ; Lung Diseases/immunology ; Lung Diseases/metabolism ; Lung Diseases/pathology ; Macrophages/immunology ; Macrophages/metabolism ; Phagocytosis/immunology ; Receptors, Cell Surface/metabolism ; Signal Transduction
Chemical Substances	Biomarkers ; Receptors, Cell Surface
Keywords	covid19
Language	English
Publishing date	2016-03-08
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	2316828-6
ISSN	1863-2300 ; 1863-2297
ISSN (online)	1863-2300
ISSN	1863-2297
DOI	10.1007/s00281-016-0555-3
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Article ; Online: Culture of Human Monocyte-Derived Macrophages.

Kelly, Aoife / Grabiec, Aleksander M / Travis, Mark A

Methods in molecular biology (Clifton, N.J.)

2018 Volume 1784, Page(s) 1–11

Abstract: The study of human macrophages is often hampered by access to tissue and inability of this cell type to survive in vitro following isolation. The culture of human monocyte-derived macrophages (MDMs) represents a tool to study macrophages, with monocytes ... ...

Abstract	The study of human macrophages is often hampered by access to tissue and inability of this cell type to survive in vitro following isolation. The culture of human monocyte-derived macrophages (MDMs) represents a tool to study macrophages, with monocytes known to give rise to tissue macrophages influenced by certain environmental cues. Here we describe a method of culturing monocyte-derived macrophages from CD14+ blood monocytes and polarization toward different macrophage phenotypes.
MeSH term(s)	Cell Culture Techniques/methods ; Cell Differentiation/genetics ; Humans ; Lipopolysaccharide Receptors/genetics ; Macrophages/cytology ; Molecular Biology/methods ; Monocytes/cytology
Chemical Substances	Lipopolysaccharide Receptors
Language	English
Publishing date	2018-05-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-7837-3_1
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