scholarly journals CX3CL1 and CX3CR1 Expressing Tendon Cells – A novel Immune Cell Population in the Tendon Core

2019 ◽  
Author(s):  
Christine Lehner ◽  
Gabriel Spitzer ◽  
Renate Gehwolf ◽  
Andrea Wagner ◽  
Nadja Weissenbacher ◽  
...  
Keyword(s):  
Cell Population ◽  
Immune Cell ◽  
Dense Matrix ◽  
Healthy Human ◽  
Immune Cell Population ◽  
Fractalkine Receptor ◽  
Tendon Cells ◽  
Human Tendon ◽  
Summary Statement

AbstractTendon disorders frequently occur and recent evidence has clearly implicated the presence of immune cells and inflammatory events during early tendinopathy. However, the origin and properties of these cells remain poorly defined. Therefore, the aim of this study was to determine the presence of myleoid cells in healthy rodent and human tendon tissue and to characterize them. Using various transgenic reporter mouse models, we demonstrate the presence of tendon cells in the dense matrix of the tendon core expressing the fractalkine (Fkn) receptor CX3CR1 and its cognate ligand CX3CL1/Fkn. Pro-inflammatory stimulation of 3D tendon-like constructsin vitroresulted in a significant increase in the expression of IL-1β, IL-6, Mmp3, Mmp9, Cx3cl1, and epiregulin which has been reported to contribute to inflammation, wound healing, and tissue repair. Furthermore, we demonstrate that inhibition of the fractalkine receptor blocked tendon cell migrationin vitroand show the presence of CX3CR1/CX3CL1/EREG expressing cells in healthy human tendons. Taken together, we demonstrate the presence of CX3CL1+/CX3CR1+ “tenophages” within the healthy tendon proper potentially fulfilling surveillance functions in tendons.Summary StatementHere, we demonstrate the presence of a macrophage-like, CX3CL1/CX3CR1-expressing cell population within the healthy tendon proper potentially fulfilling a surveillance function.

Lipocalin 2 – Devil or Angel? A pan cancer study.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15609-e15609
Author(s):  
Vijay Kumar Srinivasalu ◽  
Narayana Subramaniam ◽  
Manjula Das ◽  
Sujan Kumar Dhar
Keyword(s):  
Cell Population ◽  
Squamous Cell ◽  
Immune Cell ◽  
Tumour Progression ◽  
Migration And Invasion ◽  
Lower Grade ◽  
Lipocalin 2 ◽  
Immune Cell Population ◽  
Significant Difference

e15609 Background: Lipocalin2 (LCN2, also known as neutrophil gelatinase-associated lipocalin), is a protein that in humans is encoded by the LCN2 gene. It’s abnormal expression serves critical roles in the EMT transition process, angiogenesis, cell migration and invasion in many cancers. We aim to study the expression of LCN2 in tumours with respect to normal and its association with survival in multiple forms of cancer. Methods: On analysis of 23 TCGA datasets containing gene expression data for both tumour and adjacent normal samples, normalized RNAseq RSEM values of LCN2 were compared and differences between median expression levels were assessed using Wilcoxon rank sum test. Effect of LCN2 expression (lowest and highest tertiles) in tumour samples were estimated using Kaplan-Meier survival model. Correlation of LCN2 expression with immune cell population estimated using MCP Counter tool in Colonic Adenocarcinoma (CAC) and Head and Neck Squamous Cell Carcinoma (HNSCC) dataset were assessed. Results: LCN2 overexpression in tumour over normal was seen in 11 cancers viz. CAC, Cholangiocarcinoma, Esophageal ca, Kidney chromophobe, Kidney renal papillary cell ca, HCC, Lung adenoca, Rectum adenoca, Skin cutaneous melanoma, Thyroid ca and endometrial ca whereas LCN2 under-expression in tumour over normal was observed in 4 including HNSCC, Breast invasive ca, RCC and Prostate adenoca. For 8 cancers (Urothelial ca, Cervical and endocervical ca, Glioblastoma, Lower grade glioma, Lung squamous cell ca, Pancreatic adenoca, Phenochromocytoma and Stomach adenoca) no significant difference was observed between normal and tumour samples. LCN2 expression shows hazardous effect on OS in Renal Clear Cell ca (HR = 2.38, p = 0.00027), Glioblastoma (HR = 1.57, p = 0.036) and Pheochromocytoma (HR = 8.03, p = 0.03). On the other hand, high expression of LCN2 shows very mild protective effect on tumour progression in HNSCC (HR = 0.71, p = 0.05) and Prostate ca (HR = 0.46, p = 0.06). In CAC, the normal samples show a correlation between LCN2 expression and T-cells (Pearson r = 0.45, p = 0.0028) and with the T-cell chemo attractant CXCL10 (Pearson r = 0.5, p < 0.0001). Such correlations are broken in tumour samples. In HNSCC no correlations are visible between LCN2 expression and immune cell population estimate in either tumour or normal samples. Conclusions: Literature shows LCN2 as a potential therapeutic target. However, initial analysis of TCGA data fails to establish its role as pro- or anti-tumorigenic in multiple cancers. Further tissue-specific analysis including in vitro and invivo studies are needed to confirm its role in cancer.

scholarly journals Dexamethasone decreases substance P expression in human tendon cells: an in vitro study

Rheumatology ◽  
2014 ◽  
Vol 54 (2) ◽  
pp. 318-323 ◽  
Author(s):  
R. Mousavizadeh ◽  
L. Backman ◽  
R. G. McCormack ◽  
A. Scott
Keyword(s):  
Substance P ◽  
In Vitro Study ◽  
Vitro Study ◽  
Tendon Cells ◽  
Human Tendon

scholarly journals Reconstitution of immune cell interactions in free-standing membranes

2018 ◽  
Author(s):  
Edward Jenkins ◽  
Ana Mafalda Santos ◽  
James H. Felce ◽  
Deborah Hatherley ◽  
Michael L. Dustin ◽  
...  
Keyword(s):  
Synapse Formation ◽  
Immune Cell ◽  
Cell Interactions ◽  
Free Standing ◽  
Immune Synapse ◽  
Signalling Molecules ◽  
Transient Nature ◽  
Spatiotemporal Regulation ◽  
Summary Statement

AbstractThe spatiotemporal regulation of signalling proteins at the contacts formed between immune cells and their targets determines how and when immune responses begin and end. It is important, therefore, to be able to elucidate molecular processes occurring at these interfaces. However, the detailed investigation of each component’s contribution to the formation and regulation of the contact is hampered by the complexity of cellular composition and architecture. Moreover, the transient nature of these interactions creates additional challenges, especially for using advanced imaging technology. One approach to circumventing these problems is to establish in vitro systems that faithfully mimic immune cell interactions, incorporating complexity that can be ‘dialled-in’ as needed. Here, we present an in vitro system making use of synthetic vesicles that mimic important aspects of immune cell surfaces. Using this system, we begin to investigate the spatial distribution of signalling molecules (receptors, kinases and phosphatases) and the intracellular rearrangements that accompany the initiation of signalling in T cells. The model system presented here is expected to be widely applicable.Summary StatementImmune cell-cell interactions are reconstituted in free-standing vesicles wherein spatiotemporal aspects of immune synapse formation can be investigated.

scholarly journals Evolution during primary HIV infection does not require adaptive immune selection

2020 ◽  
Author(s):  
David A Swan ◽  
Morgane Rolland ◽  
Joshua Herbeck ◽  
Joshua T Schiffer ◽  
Daniel B Reeves
Keyword(s):  
Viral Load ◽  
Immune System ◽  
Hiv Infection ◽  
Evolutionary Dynamics ◽  
Immune Cell ◽  
Adaptive Immune System ◽  
Viral Fitness ◽  
Immune Cell Population ◽  
Adaptive Immune

AbstractModern HIV research depends crucially on both viral sequencing and population measurements. To directly link mechanistic biological processes and evolutionary dynamics during HIV infection, we developed multiple within-host phylodynamic (wi-phy) models of HIV primary infection for comparative validation against viral load and evolutionary dynamics data. The most parsimonious and accurate model required no positive selection, suggesting that the host adaptive immune system reduces viral load, but does not drive observed viral evolution. Rather, random genetic drift primarily dictates fitness changes. These results hold during early infection, and even during chronic infection when selection has been observed, viral fitness distributions are not largely different from in vitro distributions that emerge without adaptive immunity. These results highlight how phylogenetic inference must consider complex viral and immune-cell population dynamics to gain accurate mechanistic insights.One sentence summaryThrough the lens of a unified population and phylodynamic model, current data show the first wave of HIV mutations are not driven by selection by the adaptive immune system.

scholarly journals P062 Differences in immune cell population subsets in inflammatory bowel disease patients under anti-TNF treatment

2019 ◽  
Vol 13 (Supplement_1) ◽  
pp. S117-S117
Author(s):  
S Notararigo ◽  
J E Viñuela Roldán ◽  
M Abanades-Tercero ◽  
J E Dominguez-Munoz ◽  
M Barreiro-de Acosta
Keyword(s):  
Inflammatory Bowel Disease ◽  
Cell Population ◽  
Bowel Disease ◽  
Immune Cell ◽  
Immune Cell Population ◽  
Inflammatory Bowel

scholarly journals 110 Characterizing the immune cell population in the human fetal membrane

2021 ◽  
Vol 224 (2) ◽  
pp. S76-S77
Author(s):  
Sara Jacobs ◽  
Samantha Sheller-Miller ◽  
Lauren Richardson ◽  
Rheanna Urrabaz-Garza ◽  
Enkhtuya Radnaa ◽  
...  
Keyword(s):  
Cell Population ◽  
Immune Cell ◽  
Fetal Membrane ◽  
Immune Cell Population

scholarly journals Immune Cell Population in Ovarian Tumor Microenvironment

2017 ◽  
Vol 8 (15) ◽  
pp. 2915-2923 ◽  
Author(s):  
Dong Li Cai ◽  
Li-Ping Jin
Keyword(s):  
Tumor Microenvironment ◽  
Cell Population ◽  
Ovarian Tumor ◽  
Immune Cell ◽  
Immune Cell Population

Abstract 003: Cholinergic Expansion of an Inflammatory Macrophage Population in the Pre-Hypertensive Spontaneously Hypertensive Rat

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Sailesh Harwani ◽  
Mark W Chapleau ◽  
Fayyaz Sutterwala ◽  
Zuhair Ballas ◽  
David Meyerholz ◽  
...  
Keyword(s):  
Cell Population ◽  
Immune Cell ◽  
Spontaneously Hypertensive Rat ◽  
Isolated Cells ◽  
Immune Cell Population ◽  
Macrophage Population ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Wistar Kyoto ◽  
Cholinergic Activation

Our laboratory previously identified an abnormally elevated CD161a+ immune cell population in splenocytes of the pre-hypertensive Spontaneously Hypertensive Rat (SHR) that was abnormally expanded following cholinergic activation with nicotine . In the present study, we tested the hypothesis that the expanded CD161a+ cell population represents an activated monocyte/macrophage population and are present in the bone marrow (BM). We isolated cells from the spleen and BM of pre-hypertensive (4-5 week old) SHR (n=3) and age-matched normotensive Wistar Kyoto (WKY, n=3) rats. Isolated cells were stained with a fluorochrome conjugated anti-rat CD161a monoclonal antibody and analyzed by flow cytometry. CD161a+ cells were more prevalent in splenocytes and BM of the pre-hypertensive SHR, compared to WKY (8.7 ± 1.4% vs 1.2 ± 0.6% and 12.6 ± 1.8% vs 1.7 ± 0.8%, respectively, p<0.001). BM cells and splenocytes were cultured for 36-48 hours in the presence or absence of nicotine (10μM) and then stained with fluorochrome conjugated anti-rat CD161a and CD68 antibodies. CD68 is a well accepted pan-macrophage marker that is up-regulated on activated monocytes/macrophages. The CD161+/CD68+ macrophages were comparable between the WKY and SHR in freshly isolated cells from the spleen (0.3 ± 0.2% vs 0.9 ± 0.5%, respectively) and BM (0.6 ± 0.4% vs 0.7 ± 0.2%, respectively). However, nicotine strongly expanded the CD161a+/CD68+ macrophage population in the BM of the SHR (1.1 ± 0.15% to 11.9 ± 3.45%, p<0.001) and WKY (1.7 ± 0.17% to 11.0 ± 1.9%, p<0.001). In contrast, the response of splenocytes to nicotine was strong in SHR (1.8 ± 0.40% to 10.7 ± 1.1%, p<0.001), but not significant in WKY (1.9 ± 0.4% to 3.1 ± 0.6%, p>0.05). Nicotine had no effect on the CD161a+/CD68- cell population in either splenocytes or BM cells of the SHR or WKY. Thus, an activated monocyte/macrophage population (CD161a+/CD68+) is expanded by cholinergic activation in both the BM and spleen of SHR, but only in the BM and not spleen of the WKY. Since, the pro-inflammatory nicotinic response present in the BM of the WKY is abrogated in the peripheral spleen, we conclude that the retention of this response in the SHR may contribute to the development of hypertension.

Abstract A57: βhCG regulates immune cell population in BRCA1 mutated breast cancers

2020 ◽  
Author(s):  
Geetu Rose Varghese ◽  
Vishnu Sunil Jaikumar ◽  
Arathi Rajan ◽  
Neetha Rajan Latha ◽  
Dipyaman Patra ◽  
...  
Keyword(s):  
Cell Population ◽  
Immune Cell ◽  
Breast Cancers ◽  
Immune Cell Population
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