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 ◽  
...  
PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e34521 ◽  
Author(s):  
Corine St. Gelais ◽  
Christopher M. Coleman ◽  
Jian-Hua Wang ◽  
Li Wu

2002 ◽  
Vol 275 (2) ◽  
pp. 243-254 ◽  
Author(s):  
Maria Giovanna Quaranta ◽  
Elena Tritarelli ◽  
Luciana Giordani ◽  
Marina Viora

Blood ◽  
2003 ◽  
Vol 102 (5) ◽  
pp. 1745-1752 ◽  
Author(s):  
Keith Crawford ◽  
Aleksandra Stark ◽  
Betsy Kitchens ◽  
Kerry Sternheim ◽  
Vassilios Pantazopoulos ◽  
...  

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.


2009 ◽  
Vol 5 (1) ◽  
pp. e1000279 ◽  
Author(s):  
Takuya Yamamoto ◽  
Yasuko Tsunetsugu-Yokota ◽  
Yu-ya Mitsuki ◽  
Fuminori Mizukoshi ◽  
Takatsugu Tsuchiya ◽  
...  

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Liang Xiao ◽  
Annet Kirabo ◽  
David G Harrison

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.


2003 ◽  
Vol 13 (1) ◽  
pp. 69-78 ◽  
Author(s):  
Xianghong Zhou ◽  
James G. Krueger ◽  
Ming-Chih J. Kao ◽  
Ed Lee ◽  
Fenghe Du ◽  
...  

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.


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