scholarly journals Enhanced CD4+ T Cell Proliferation and Th2 Cytokine Production in DR6-Deficient Mice

Immunity ◽  
2001 ◽  
Vol 15 (1) ◽  
pp. 23-34 ◽  
Author(s):  
Jinqi Liu ◽  
Songqing Na ◽  
Andrew Glasebrook ◽  
Niles Fox ◽  
Patricia J. Solenberg ◽  
...  
2002 ◽  
Vol 168 (1) ◽  
pp. 118-126 ◽  
Author(s):  
S. Christine Henderson ◽  
Mihir M. Kamdar ◽  
Anil Bamezai

2008 ◽  
Vol 129 (1) ◽  
pp. 80-89 ◽  
Author(s):  
Chris J. Hedegaard ◽  
Martin Krakauer ◽  
Klaus Bendtzen ◽  
Per Soelberg Sørensen ◽  
Finn Sellebjerg ◽  
...  

2017 ◽  
Vol 8 ◽  
Author(s):  
Shannon M. Lange ◽  
Melanie C. McKell ◽  
Stephanie M. Schmidt ◽  
Austin P. Hossfeld ◽  
Vandana Chaturvedi ◽  
...  

Author(s):  
S. Laurent ◽  
P. Carrega ◽  
D. Saverino ◽  
P. Piccioli ◽  
M. Camoriamo ◽  
...  

<p>CTLA-4 is the major nefative regulator of T cell response. We have analyzed the expression of CTLA-4 in human monocytes and monocyte-derived DCs and the effects of its engagement on cytokine production and T cell stimulatory activity by mature DCs (mDCs). We found the CTLA-4 was highly expressed on freshly isolated monocytes, then down-modulated on the immature DCs (iDCs) and upregulated on mDCs. Treatment of mDCS with an agonistic anti-CTLA-4 m Ab enhanced secretion of IL-10 but reduced secretion of IL-8 and IL-12, as well as autologous CD4* T-cell proliferation in response to simulation with PPD recall antigenloaded-DCs. Neutralization of IL-10 with an anti-IL-10 antibody partially restored the ability of anti-CTLA-4-treated mDCs to stimulate T cell proliferation in response to PPD. Our data provide the first evidence that CTLA-4 receptor is expressed by human mDCs and exerts immune modulatory effects in these cells.</p>


2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Lucas Faustino ◽  
Daniel Mucida ◽  
Alexandre Castro Keller ◽  
Jocelyne Demengeot ◽  
Karina Bortoluci ◽  
...  

Foxp3+CD25+CD4+regulatory T cells are vital for peripheral tolerance and control of tissue inflammation. In this study, we characterized the phenotype and monitored the migration and activity of regulatory T cells present in the airways of allergic or tolerant mice after allergen challenge. To induce lung allergic inflammation, mice were sensitized twice with ovalbumin/aluminum hydroxide gel and challenged twice with intranasal ovalbumin. Tolerance was induced by oral administration of ovalbumin for 5 consecutive days prior to OVA sensitization and challenge. We detected regulatory T cells (Foxp3+CD25+CD4+T cells) in the airways of allergic and tolerant mice; however, the number of regulatory T cells was more than 40-fold higher in allergic mice than in tolerant mice. Lung regulatory T cells expressed an effector/memory phenotype (CCR4highCD62LlowCD44highCD54highCD69+) that distinguished them from naive regulatory T cells (CCR4intCD62LhighCD44intCD54intCD69−). These regulatory T cells efficiently suppressed pulmonary T-cell proliferation but not Th2 cytokine production.


Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1606
Author(s):  
Peter Seiringer ◽  
Stefanie Eyerich ◽  
Kilian Eyerich ◽  
Daniela Dittlein ◽  
Anna Caroline Pilz ◽  
...  

Whilst the importance of keratinocytes as a first-line defense has been widely investigated, little is known about their interactions with non-resident immune cells. In this study, the impact of human keratinocytes on T cell effector functions was analyzed in an antigen-specific in vitro model of allergic contact dermatitis (ACD) to nickel sulfate. Keratinocytes partially inhibited T cell proliferation and cytokine production. This effect was dependent on the keratinocyte/T cell ratio and was partially reversible by increasing the number of autologous dendritic cells. The inhibition of T cell proliferation by keratinocytes was independent of the T cell subtype and antigen presentation by different professional antigen-presenting cells. Autologous and heterologous keratinocytes showed comparable effects, while the fixation of keratinocytes with paraformaldehyde abrogated the immunosuppressive effect. The separation of keratinocytes and T cells by a transwell chamber, as well as a cell-free keratinocyte supernatant, inhibited T cell effector functions to the same amount as directly co-cultured keratinocytes, thus proving that soluble factor/s account for the observed suppressive effects. In conclusion, keratinocytes critically control the threshold of inflammatory processes in the skin by inhibiting T cell proliferation and cytokine production.


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