scholarly journals Renal denervation prevents dendritic cell activation and renal T cell activation in mice in angiotensin II‐induced hypertension (1082.4)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Liang Xiao ◽  
Annet Kirabo ◽  
Jing Wu ◽  
David Harrison
Keyword(s):  
T Cell ◽  
Angiotensin Ii ◽  
Dendritic Cell ◽  
T Cell Activation ◽  
Renal Denervation ◽  
Cell Activation ◽  
Dendritic Cell Activation ◽  
Induced Hypertension

Abstract 60: Renal Denervation Prevents Dendritic Cell Activation and Renal T Cell Activation in Mice During Angiotensin Ii-induced Hypertension

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Liang Xiao ◽  
Annet Kirabo ◽  
David G Harrison
Keyword(s):  
Blood Pressure ◽  
T Cells ◽  
T Cell ◽  
Angiotensin Ii ◽  
Dendritic Cell ◽  
T Cell Activation ◽  
Renal Denervation ◽  
Cell Activation ◽  
Sympathetic Nerves ◽  
Dendritic Cell Activation

Increased sympathetic outflow has been implicated in the pathogenesis of hypertension. Recent evidence has also suggested a role of T lymphocytes in hypertension. Renal sympathectomy is an effective approach to lower blood pressure in hypertensive patients and animal models. We hypothesized that renal sympathetics link the central nervous system to immune activation in hypertension. To test this hypothesis, we performed either unilateral or bilateral renal denervation (DNX) in C57BL/6 mice by applying phenol to the renal artery and cutting large visible nerves. On the same day mice received an osmotic minipump for angiotensin II (ANG) infusion (490 ng/kg/min, for 14 days). DNX decreased renal norepinephrine content from 162±13 to 42±11 ng/g (p=0.005) as measured by HPLC. Bilateral DNX lowered systolic blood pressure in mice with ANG infusion (137±4 vs. 159±5 mmHg, p=0.003) measured with tail-cuff. Analysis of T cells was performed using flow cytometry in single cell suspensions from kidneys. Angiotensin II significantly increased total leukocyte (CD45+) and T cell (CD3+) infiltration in the kidney, and this was prevented by DNX. Dendritic cells (DCs), which are the major antigen presenting cells that activate T cells, were isolated from the spleen and cultured in RPMI medium for 24 hours for cytokine measurements via Luminex100 system. Angiotensin II infusion increased DC production in IL-1α, IL-1β, and IL-6 production by 4 to 6-fold, and these increases were prevented by DNX. These results suggest that renal sympathetic nerves participate in T cell activation, and this is associated with dendritic cell activation in the spleen.

scholarly journals Gut dendritic cell activation links an altered colonic microbiome to mucosal and systemic T-cell activation in untreated HIV-1 infection

2015 ◽  
Vol 9 (1) ◽  
pp. 24-37 ◽  
Author(s):  
S M Dillon ◽  
E J Lee ◽  
C V Kotter ◽  
G L Austin ◽  
S Gianella ◽  
...  
Keyword(s):  
T Cell ◽  
Dendritic Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Dendritic Cell Activation ◽  
Hiv 1

Abstract 023: γδ T Cells Mediate αβ T Cell Activation in Angiotensin II-Induced Hypertension

Hypertension ◽  
2019 ◽  
Vol 74 (Suppl_1) ◽  
Author(s):  
Antoine Caillon ◽  
Pierre Paradis ◽  
Ernesto L Schiffrin
Keyword(s):  
T Cells ◽  
T Cell ◽  
Angiotensin Ii ◽  
T Cell Activation ◽  
Cell Activation ◽  
Γδ T Cells ◽  
Induced Hypertension

CD2 engagement induces dendritic cell activation: implications for immune surveillance and T-cell activation

Blood ◽  
2003 ◽  
Vol 102 (5) ◽  
pp. 1745-1752 ◽  
Author(s):  
Keith Crawford ◽  
Aleksandra Stark ◽  
Betsy Kitchens ◽  
Kerry Sternheim ◽  
Vassilios Pantazopoulos ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
Dendritic Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Immune Surveillance ◽  
T Cell Proliferation ◽  
Dendritic Cell Activation ◽  
Adaptive Immune

Abstract We have shown previously that primary dendritic cells and monocytes express equal levels of CD14 but are distinguishable by the presence of CD2 on dendritic cells. CD2 is known to mediate the activation of T and natural killer (NK) cells through its interaction with CD58. CD2 epitopes recognized by anti-T111, -T112, and -T113 monoclonal antibodies (mAbs) are present on dendritic cells. Here we show that CD2 engagement significantly increases class II, costimulatory (CD40, CD80, CD86), adhesion (CD54, CD58), and CCR7 molecule expression on primary dendritic cells. Conversely, minimal or no change in the expression of the above antigens occurs on monocyte-derived dendritic cells, because these molecules are already maximally expressed. However, both kinds of dendritic cells release interleukin-1β (IL-1β) and IL-12 after CD2 engagement. Lastly, interference with dendritic cell CD2–T-cell CD58 engagement decreases naive CD4+CD45RA+ T-cell proliferation. Collectively, our results suggest another role of the CD2-CD58 pathway that allows nonimmune and immune cells to interact directly with dendritic cells and initiate innate and adaptive immune responses.

Novel mechanisms of T-cell and dendritic cell activation revealed by profiling of psoriasis on the 63,100-element oligonucleotide array

2003 ◽  
Vol 13 (1) ◽  
pp. 69-78 ◽  
Author(s):  
Xianghong Zhou ◽  
James G. Krueger ◽  
Ming-Chih J. Kao ◽  
Ed Lee ◽  
Fenghe Du ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Dendritic Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Spatial Organization ◽  
Oligonucleotide Array ◽  
Dendritic Cell Activation ◽  
Activation Markers ◽  
Cytokines And Chemokines

A global picture of gene expression in the common immune-mediated skin disease, psoriasis, was obtained by interrogating the full set of Affymetrix GeneChips with psoriatic and control skin samples. We identified 1,338 genes with potential roles in psoriasis pathogenesis/maintenance and revealed many perturbed biological processes. A novel method for identifying transcription factor binding sites was also developed and applied to this dataset. Many of the identified sites are known to be involved in immune response and proliferation. An in-depth study of immune system genes revealed the presence of many regulating cytokines and chemokines within involved skin, and markers of dendritic cell (DC) activation in uninvolved skin. The combination of many CCR7+ T cells, DCs, and regulating chemokines in psoriatic lesions, together with the detection of DC activation markers in nonlesional skin, strongly suggests that the spatial organization of T cells and DCs could sustain chronic T-cell activation and persistence within focal skin regions.

Abstract 242: Superoxide and Isoketal Neo-antigen formation in Dendritic Cells from Hypertensive mice activate T cells and promote Hypertension

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Annet Kirabo ◽  
Jing Wu ◽  
Salim R Thabet ◽  
Alfiya T Bikineyeva ◽  
Sergey Dikalov ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Angiotensin Ii ◽  
T Cell Activation ◽  
Cell Activation ◽  
Superoxide Production ◽  
Blood Pressure Elevation ◽  
Induced Hypertension ◽  
Endogenous Proteins

Superoxide and inflammation contribute to the genesis of hypertension but the mechanisms involved are not fully understood. We examined the hypothesis that oxidative stress in dendritic cells (DCs) alters endogenous proteins via Isoketal-modification leading to formation of neo-antigens, T cell activation and blood pressure elevation. DCs isolated from mice with angiotensin II-induced hypertension had a significant increase in NADPH oxidase-dependent superoxide production when compared to sham-treated mice (334.0±49.7 versus 65.8±4.5 pmol/mg protein). This was associated with an exuberant DC accumulation of protein-isoketal adducts and activation of IL-6, IL-1β and IL-23 production. DCs from hypertensive mice but not sham mice promoted survival and proliferation of CD8 + T cells in culture. Scavenging of isoketals not only prevented activation and immunogenicity of DCs, but also markedly attenuated angiotensin II-induced hypertension (142.59 ± 8.98 mmHg versus 175.53 ± 5.19 mmHg in controls). Moreover, adaptive transfer of DCs from hypertensive mice primed development of hypertension in mice given a sub-pressor dose of angiotensin II (157.45 ± 33.86 mmHg versus 119.90 ± 17.33 mmHg in controls). These studies show that angiotensin II-induced hypertension activates DCs, in large part by causing superoxide production and formation of isoketals. We propose that Isoketal-modified proteins can be presented as neo-antigens by DCs, which in turn trigger T cell activation leading to hypertension.

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