Synthetic nanoparticles that promote tumor necrosis factor receptor 2 expressing regulatory T cells in the lung and resistance to allergic airways inflammation

Rohimah Mohamud, Jeanne S. LeMasurier, Jennifer C. Boer, Je Lin Sieow, Jennifer M. Rolland, Robyn E. O'Hehir, Charles L. Hardy, Magdalena Plebanski

Research output: Contribution to journalArticleResearchpeer-review

3 Citations (Scopus)

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 languageEnglish
Article number1812
JournalFrontiers in Immunology
Volume8
Issue numberDEC
DOIs
Publication statusPublished - 22 Dec 2017

Keywords

  • Animal model
  • Asthma
  • Lung
  • Lymph nodes
  • Nanoparticles
  • PS50G
  • Tumor necrosis factor 2

Cite this

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title = "Synthetic nanoparticles that promote tumor necrosis factor receptor 2 expressing regulatory T cells in the lung and resistance to allergic airways inflammation",
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.",
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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 journalArticleResearchpeer-review

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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

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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.

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