scholarly journals Natural Tr1-like cells do not confer long-term tolerogenic memory

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Koshika Yadava ◽  
Carlos Obed Medina ◽  
Heather Ishak ◽  
Irina Gurevich ◽  
Hedwich Kuipers ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Memory T Cell ◽  
Egfp Reporter ◽  
Dust Mite ◽  
Primary Sensitization ◽  
Phenotypic Instability ◽  
Tr1 Cells

IL-10-producing Tr1 cells promote tolerance but their contributions to tolerogenic memory are unclear. Using 10BiT mice that carry a Foxp3-eGFP reporter and stably express CD90.1 following IL-10 production, we characterized the spatiotemporal dynamics of Tr1 cells in a house dust mite model of allergic airway inflammation. CD90.1+Foxp3-IL-10+ Tr1 cells arise from memory cells and rejoin the tissue-resident memory T-cell pool after cessation of IL-10 production. Persistent antigenic stimulation is necessary to sustain IL-10 production and Irf1 and Batf expression distinguishes CD90.1+Foxp3-IL-10+ Tr1 cells from CD90.1+Foxp3-IL-10- ‘former’ Tr1. Depletion of Tr1-like cells after primary sensitization exacerbates allergic airway inflammation. However, neither transfer nor depletion of former Tr1 cells influences either Tr1 numbers or the inflammatory response during subsequent allergen memory re-challenge weeks later. Together these data suggest that naturally-arising Tr1 cells do not necessarily give rise to more Tr1 upon allergen re-challenge or contribute to tolerogenic memory. This phenotypic instability may limit efforts to re-establish tolerance by expanding Tr1 in vivo.

scholarly journals Allergin-1 Immunoreceptor Suppresses House Dust Mite–Induced Allergic Airway Inflammation

2020 ◽  
Vol 204 (4) ◽  
pp. 753-762 ◽  
Author(s):  
Haruka Miki ◽  
Satoko Tahara-Hanaoka ◽  
Mariana Silva Almeida ◽  
Kaori Hitomi ◽  
Shohei Shibagaki ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
House Dust ◽  
House Dust Mite ◽  
Allergic Airway Inflammation ◽  
Dust Mite

scholarly journals Ingestion of milk containing the Dp2 peptide, a dust mite allergen, protects mice from allergic airway inflammation and hyper-responsiveness

2013 ◽  
Vol 9 (1) ◽  
pp. 21 ◽  
Author(s):  
Hsu-Chung Liu ◽  
Shun-Yuan Pai ◽  
Winston TK Cheng ◽  
Hsiao-Ling Chen ◽  
Tung-Chou Tsai ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Mite Allergen ◽  
Dust Mite ◽  
Dust Mite Allergen

scholarly journals IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models

2017 ◽  
Vol 214 (10) ◽  
pp. 3037-3050 ◽  
Author(s):  
Takashi Ito ◽  
Koichi Hirose ◽  
Aiko Saku ◽  
Kenta Kono ◽  
Hiroaki Takatori ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
House Dust ◽  
House Dust Mite ◽  
Cytokine Production ◽  
Allergic Airway Inflammation ◽  
Lung Epithelial Cells ◽  
Intratracheal Administration ◽  
Lung Epithelial ◽  
Dust Mite

Previous studies have shown that IL-22, one of the Th17 cell–related cytokines, plays multiple roles in regulating allergic airway inflammation caused by antigen-specific Th2 cells; however, the underlying mechanism remains unclear. Here, we show that allergic airway inflammation and Th2 and Th17 cytokine production upon intratracheal administration of house dust mite (HDM) extract, a representative allergen, were exacerbated in IL-22-deficient mice. We also found that IL-22 induces Reg3γ production from lung epithelial cells through STAT3 activation and that neutralization of Reg3γ significantly exacerbates HDM-induced eosinophilic airway inflammation and Th2 cytokine induction. Moreover, exostatin-like 3 (EXTL3), a functional Reg3γ binding protein, is expressed in lung epithelial cells, and intratracheal administration of recombinant Reg3γ suppresses HDM-induced thymic stromal lymphopoietin and IL-33 expression and accumulation of type 2 innate lymphoid cells in the lung. Collectively, these results suggest that IL-22 induces Reg3γ production from lung epithelial cells and inhibits the development of HDM-induced allergic airway inflammation, possibly by inhibiting cytokine production from lung epithelial cells.

scholarly journals HDAC2 attenuates airway inflammation by suppressing IL-17A production in HDM-challenged mice

2019 ◽  
Vol 316 (1) ◽  
pp. L269-L279 ◽  
Author(s):  
Tianwen Lai ◽  
Mindan Wu ◽  
Chao Zhang ◽  
Luanqing Che ◽  
Feng Xu ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Inflammatory Cells ◽  
Protective Role ◽  
In Vivo Models

Histone deacetylase (HDAC)2 is expressed in airway epithelium and plays a pivotal role in inflammatory cells. However, the role of HDAC2 in allergic airway inflammation remains poorly understood. In the present study, we determined the role of HDAC2 in airway inflammation using in vivo models of house dust mite (HDM)-induced allergic inflammation and in vitro cultures of human bronchial epithelial (HBE) cells exposed to HDM, IL-17A, or both. We observed that HDM-challenged Hdac2+/− mice exhibited substantially enhanced infiltration of inflammatory cells. Higher levels of T helper 2 cytokines and IL-17A expression were found in lung tissues of HDM-challenged Hdac2+/− mice. Interestingly, IL-17A deletion or anti-IL-17A treatment reversed the enhanced airway inflammation induced by HDAC2 impairment. In vitro, HDM and IL-17A synergistically decreased HDAC2 expression in HBE cells. HDAC2 gene silencing further enhanced HDM- and/or IL-17A-induced inflammatory cytokines in HBE cells. HDAC2 overexpresion or blocking IL-17A gene expression restored the enhanced inflammatory cytokines. Collectively, these results support a protective role of HDAC2 in HDM-induced airway inflammation by suppressing IL-17A production and might suggest that activation of HDAC2 and/or inhibition of IL-17A production could prevent the development of allergic airway inflammation.

scholarly journals β2 adrenergic agonist attenuates house dust mite-induced allergic airway inflammation through dendritic cells

2014 ◽  
Vol 15 (1) ◽  
Author(s):  
Go Kato ◽  
Koichiro Takahashi ◽  
Hiroki Tashiro ◽  
Keigo Kurata ◽  
Hideharu Shirai ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Airway Inflammation ◽  
House Dust ◽  
House Dust Mite ◽  
Allergic Airway Inflammation ◽  
Adrenergic Agonist ◽  
Dust Mite

scholarly journals An in Vitro and in Vivo Study of the Effect of Dexamethasone on Immunoinhibitory Function of Induced Pluripotent Stem Cell-Derived Mesenchymal Stem Cells

2018 ◽  
Vol 27 (9) ◽  
pp. 1340-1351 ◽  
Author(s):  
Dan Wang ◽  
Yue-Qi Sun ◽  
Wen-Xiang Gao ◽  
Xing-Liang Fan ◽  
Jian-Bo Shi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Airway Inflammation ◽  
Pluripotent Stem Cell ◽  
Allergic Airway Inflammation ◽  
Induced Pluripotent Stem Cell ◽  
Induced Pluripotent ◽  
Immunomodulatory Function

Induced pluripotent stem cell-derived mesenchymal stem cells (iPSC-MSCs) represent a promising cell source for patient-specific cell therapy. We previously demonstrated that they display an immunomodulatory effect on allergic airway inflammation. Glucocorticoids are powerful anti-inflammatory compounds and widely used in the therapy of allergic diseases. However, the effect of glucocorticoids on the immunomodulatory function of iPSC-MSCs remains unknown. This study aimed to determine the effect of dexamethasone (Dex) on the immunomodulatory function of iPSC-MSCs in vitro and in vivo. A total of three human iPSC-MSC clones were generated from amniocyte-derived iPSCs. Anti-CD3/CD28-induced peripheral blood mononuclear cell (PBMC) proliferation was used to assess the effect of Dex on the immunoinhibitory function of iPSC-MSCs in vitro. Mouse models of contact hypersensitivity (CHS) and allergic airway inflammation were induced, and the levels of inflammation in mice were analyzed with the treatments of iPSC-MSCs and Dex, alone and combined. The results showed that Dex did not interfere with the immunoinhibitory effect of iPSC-MSCs on PBMC proliferation. In CHS mice, simultaneous treatment with Dex did not affect the effect of iPSC-MSCs on the inflammation, both in regional draining lymph nodes and in inflamed ear tissue. In addition, co-administration of iPSC-MSCs with Dex decreased the local expression of interferon (IFN)-γ and tumor necrosis factor (TNF)-α in the ears of CHS mice. In the mouse model of allergic airway inflammation, iPSC-MSC treatment combined with Dex resulted in a similar extent of reduction in pulmonary inflammation as iPSC-MSCs or Dex treatment alone. In conclusion, Dex does not significantly affect the immunomodulatory function of iPSC-MSCs both in vitro and in vivo. These findings may have implications when iPSC-MSCs and glucocorticoids are co-administered.

scholarly journals Frontline Science: RIP2 promotes house dust mite-induced allergic airway inflammation

2018 ◽  
Vol 104 (3) ◽  
pp. 447-459 ◽  
Author(s):  
Madelyn H. Miller ◽  
Michael G. Shehat ◽  
Karel P. Alcedo ◽  
Lina P. Spinel ◽  
Julia Soulakova ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
House Dust ◽  
House Dust Mite ◽  
Allergic Airway Inflammation ◽  
Dust Mite
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