Abstract
Synthetic glycine coated 50 nm polystyrene nanoparticles (NP) (PS50G), unlike ambient NP, do not promote pulmonary inflammation, but instead, render lungs resistant to the development of allergic airway inflammation. In this study, we show that PS50G modulate the frequency and phenotype of regulatory T cells (Treg) in the lung, specifically increasing the proportion of tumor necrosis factor 2 (TNFR2) expressing Treg. Mice pre-exposed to PS50G, which were sensitized and then challenged with an allergen a month later, preferentially expanded TNFR2+Foxp3+ Treg, which further expressed enhanced levels of latency associated peptide and cytotoxic T-lymphocyte associated molecule-4. Moreover, PS50G-induced CD103+ dendritic cell activation in the lung was associated with the proliferative expansion of TNFR2+Foxp3+ Treg. These findings provide the first evidence that engineered NP can promote the selective expansion of maximally suppressing TNFR2+Foxp3+ Treg and further suggest a novel mechanism by which NP may promote healthy lung homeostasis.
| Original language | English |
|---|---|
| Article number | 1812 |
| Journal | Frontiers in Immunology |
| Volume | 8 |
| Issue number | DEC |
| DOIs | |
| Publication status | Published - 22 Dec 2017 |
Keywords
- Animal model
- Asthma
- Lung
- Lymph nodes
- Nanoparticles
- PS50G
- Tumor necrosis factor 2
Cite this
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Synthetic nanoparticles that promote tumor necrosis factor receptor 2 expressing regulatory T cells in the lung and resistance to allergic airways inflammation. / Mohamud, Rohimah; LeMasurier, Jeanne S.; Boer, Jennifer C.; Sieow, Je Lin; Rolland, Jennifer M.; O'Hehir, Robyn E.; Hardy, Charles L.; Plebanski, Magdalena.
In: Frontiers in Immunology, Vol. 8, No. DEC, 1812, 22.12.2017.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Synthetic nanoparticles that promote tumor necrosis factor receptor 2 expressing regulatory T cells in the lung and resistance to allergic airways inflammation
AU - Mohamud, Rohimah
AU - LeMasurier, Jeanne S.
AU - Boer, Jennifer C.
AU - Sieow, Je Lin
AU - Rolland, Jennifer M.
AU - O'Hehir, Robyn E.
AU - Hardy, Charles L.
AU - Plebanski, Magdalena
PY - 2017/12/22
Y1 - 2017/12/22
N2 - Synthetic glycine coated 50 nm polystyrene nanoparticles (NP) (PS50G), unlike ambient NP, do not promote pulmonary inflammation, but instead, render lungs resistant to the development of allergic airway inflammation. In this study, we show that PS50G modulate the frequency and phenotype of regulatory T cells (Treg) in the lung, specifically increasing the proportion of tumor necrosis factor 2 (TNFR2) expressing Treg. Mice pre-exposed to PS50G, which were sensitized and then challenged with an allergen a month later, preferentially expanded TNFR2+Foxp3+ Treg, which further expressed enhanced levels of latency associated peptide and cytotoxic T-lymphocyte associated molecule-4. Moreover, PS50G-induced CD103+ dendritic cell activation in the lung was associated with the proliferative expansion of TNFR2+Foxp3+ Treg. These findings provide the first evidence that engineered NP can promote the selective expansion of maximally suppressing TNFR2+Foxp3+ Treg and further suggest a novel mechanism by which NP may promote healthy lung homeostasis.
AB - Synthetic glycine coated 50 nm polystyrene nanoparticles (NP) (PS50G), unlike ambient NP, do not promote pulmonary inflammation, but instead, render lungs resistant to the development of allergic airway inflammation. In this study, we show that PS50G modulate the frequency and phenotype of regulatory T cells (Treg) in the lung, specifically increasing the proportion of tumor necrosis factor 2 (TNFR2) expressing Treg. Mice pre-exposed to PS50G, which were sensitized and then challenged with an allergen a month later, preferentially expanded TNFR2+Foxp3+ Treg, which further expressed enhanced levels of latency associated peptide and cytotoxic T-lymphocyte associated molecule-4. Moreover, PS50G-induced CD103+ dendritic cell activation in the lung was associated with the proliferative expansion of TNFR2+Foxp3+ Treg. These findings provide the first evidence that engineered NP can promote the selective expansion of maximally suppressing TNFR2+Foxp3+ Treg and further suggest a novel mechanism by which NP may promote healthy lung homeostasis.
KW - Animal model
KW - Asthma
KW - Lung
KW - Lymph nodes
KW - Nanoparticles
KW - PS50G
KW - Tumor necrosis factor 2
UR - http://www.scopus.com/inward/record.url?scp=85038908390&partnerID=8YFLogxK
U2 - 10.3389/fimmu.2017.01812
DO - 10.3389/fimmu.2017.01812
M3 - Article
VL - 8
JO - Frontiers in Immunology
JF - Frontiers in Immunology
SN - 1664-3224
IS - DEC
M1 - 1812
ER -