scholarly journals Poly(trimethylene carbonate) and poly(D,L-lactic acid) modify human dendritic cell responses to staphylococci but do not affect Th1 and Th2 cell development

2018 ◽  
Vol 35 ◽  
pp. 103-116 ◽  
Author(s):  
PPS Balraadjsing ◽  
EC de Jong ◽  
DW Grijpma ◽  
MWT Tanck ◽  
SAJ Zaat
2020 ◽  
Vol 8 (12) ◽  
pp. 1554-1567
Author(s):  
Deena M. Maurer ◽  
Juraj Adamik ◽  
Patricia M. Santos ◽  
Jian Shi ◽  
Michael R. Shurin ◽  
...  

2020 ◽  
Vol 217 (7) ◽  
Author(s):  
Kun He ◽  
Angela Hettinga ◽  
Sagar Laxman Kale ◽  
Sanmei Hu ◽  
Markus M. Xie ◽  
...  

A Th2 immune response is central to allergic airway inflammation, which afflicts millions worldwide. However, the mechanisms that augment GATA3 expression in an antigen-primed developing Th2 cell are not well understood. Here, we describe an unexpected role for Blimp-1, a transcriptional repressor that constrains autoimmunity, as an upstream promoter of GATA3 expression that is critical for Th2 cell development in the lung to inhaled but not systemically delivered allergens but is dispensable for TFH function and IgE production. Mechanistically, Blimp-1 acts through Bcl6, leading to increased GATA3 expression in lung Th2 cells. Surprisingly, the anti-inflammatory cytokine IL-10, but not the pro-inflammatory cytokines IL-6 or IL-21, is required via STAT3 activation to up-regulate Blimp-1 and promote Th2 cell development. These data reveal a hitherto unappreciated role for an IL-10–STAT3–Blimp-1 circuit as an initiator of an inflammatory Th2 response in the lung to allergens. Thus, Blimp-1 in a context-dependent fashion can drive inflammation by promoting rather than terminating effector T cell responses.


2016 ◽  
Vol 46 (5) ◽  
pp. 1162-1167 ◽  
Author(s):  
Wei Wu ◽  
Hou-Pu Liu ◽  
Feidi Chen ◽  
Han Liu ◽  
Anthony T. Cao ◽  
...  

2019 ◽  
Author(s):  
Kun He ◽  
Angela Hettinga ◽  
Sagar Laxman Kale ◽  
Sanmei Hu ◽  
Markus M. Xie ◽  
...  

AbstractA Th2 immune response is central to allergic airway inflammation, which afflicts millions worldwide. However, the mechanisms that augment GATA3 expression in an antigen-primed developing Th2 cell are not well understood. Here, we describe an unexpected role for Blimp-1, a transcriptional repressor that constrains autoimmunity, as an upstream promoter of GATA3 expression that is critical for Th2 cell development in the lung, but dispensable for TFH function and IgE production. Mechanistically, Blimp-1 acts through Bcl6, which is necessary to drive GATA3 expression. Surprisingly, the anti-inflammatory cytokine IL-10, but not the pro-inflammatory cytokines IL-6 or IL-21, is required via STAT3 activation to upregulate Blimp-1 and promote Th2 cell development. These data reveal a hitherto unappreciated role for an IL-10-STAT3-Blimp-1 circuit as an initiator of an inflammatory Th2 response in the lung to allergens. Thus, Blimp-1 in a context-dependent fashion can drive inflammation by promoting rather than terminating effector T cell responses.SummaryThe transcriptional repressor Blimp-1 acts via a pro-inflammatory IL-10-STAT3 axis as a critical positive regulator of Th2 cells in the lung in response to allergens driving pathophysiology associated with asthma disease.


2021 ◽  
Vol 5 (2) ◽  
pp. 81-89
Author(s):  
Tanya M. Jelacic ◽  
Wilson J. Ribot ◽  
Steven A. Tobery ◽  
Donald J. Chabot ◽  
Arthur M. Friedlander

Author(s):  
Mariarosaria Marinaro ◽  
Hiroshi Kiyono ◽  
John L. VanCott ◽  
Nobuo Okahashi ◽  
Frederik W. van Ginkel ◽  
...  

Vaccine ◽  
1994 ◽  
Vol 12 (10) ◽  
pp. 903-911 ◽  
Author(s):  
Jiangchun Xu-Amano ◽  
Raymond J. Jackson ◽  
Kohtaro Fujihashi ◽  
Hiroshi Kiyono ◽  
Herman F. Staats ◽  
...  

2019 ◽  
Vol 22 ◽  
pp. 122-130 ◽  
Author(s):  
Katsuhiko Matsui ◽  
Azusa Kashima ◽  
Ayaka Motegi

Background: It is widely acknowledged that Langerhans cells (LCs) play a primary role in the polarization of T helper type 1 (Th1) or T helper type 2 (Th2) immune responses. Our aim was to find fluoroquinolone (“new quinolone”) antibiotics that would inhibit LC-mediated Th2 cell development. Methods: Expression of LC surface molecules was investigated using the reverse transcriptase polymerase chain reaction. The effects of fluoroquinolone antibiotics on T-cell immunoglobulin and mucin domain-containing protein (TIM)-4 expression in LCs were examined to predict whether they would inhibit Th2 cell development. Mice were primed via the hind footpad with ovalbumin (OVA) peptide-pulsed LCs that had been treated with a selected fluoroquinolone antibiotic, then 5 days later the cytokine response in popliteal lymph nodes was examined by enzyme-linked immunosorbent assay. Results: Norfloxacin was selected as a candidate inhibitor of Th2 cell development. As expected, OVA peptide-pulsed LCs that had been treated with norfloxacin and injected into the hind footpads of mice inhibited Th2 cell development, as represented by down-regulation of interleukin (IL)-4 production, as well as Th1 cell development, as represented by down-regulation of interferon (IFN)- g production. This additional inhibition of Th1 cell development was accompanied by suppression of CD40 expression in LCs. In addition, Staphylococcus aureus strains isolated from skin lesions of patients with atopic dermatitis (AD) were more susceptible to norfloxacin than to gentamicin. Topical treatment with norfloxacin significantly suppressed the increase in the skin severity score in NC/Nga mice with AD-like skin lesions. This suppressive effect was associated with a decrease in the production of IFN-g and IL-4 in auricular lymph node cells. Conclusions: The present results show that topical application of norfloxacin inhibits the development of AD-like skin lesions in NC/Nga mice. This suggests that topical application of norfloxacin to AD lesions colonized with S. aureus would act on both superficial S. aureus and epidermal LCs, thus possibly inhibiting the development of Th1 and Th2 cells in vivo, and controlling the severity of AD.


Immunobiology ◽  
2009 ◽  
Vol 214 (9-10) ◽  
pp. 843-851 ◽  
Author(s):  
Elisabeth Zinser ◽  
Susanne Rößner ◽  
Leonie Littmann ◽  
Daniel Lüftenegger ◽  
Ulrich Schubert ◽  
...  

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