Increased TREM-2 expression on the subsets of CD11c+ cells in the lungs and lymph nodes during allergic airway inflammation

Sannette C. Hall, Devendra K. Agrawal

Research output: Contribution to journalArticle

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Abstract

Dendritic cells (DCs) are professional APCs that traffic to the draining lymph nodes where they present processed antigens to naive T-cells. The recently discovered triggering receptor expressed on myeloid cells (TREM)-2 has been shown to be expressed on DCs in several disease models, however, its role in asthma is yet to be elucidated. In the present study, we examined the effect of allergen exposure on TREM-2 expression in the airways and on DC subsets in the lung and lymph nodes in murine model of allergic airway inflammation. Sensitization and challenge with ovalbumin reproduced hallmark features of asthma. TREM-2 mRNA expression in the whole lung was significantly higher in the OVA-sensitized and-challenged mice which was associated with increased protein expression in the lungs. Analysis of CD11c+MHC-IIhi DCs in the lung and draining lymph nodes revealed that allergen exposure increased TREM-2 expression on all DC subsets with significantly higher expression in the lymph nodes. This was associated with increased mRNA expression of Th2 and Th17 cytokines. Further analyses showed that these TREM-2+ cells expressed high levels of CCR-7 and CD86 suggesting a potential role of TREM-2 in mediating maturation and migration of DC subsets in allergic airway inflammation.

Original languageEnglish (US)
Article number11853
JournalScientific Reports
Volume7
Issue number1
DOIs
StatePublished - Dec 1 2017

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Myeloid Cells
Dendritic Cells
Lymph Nodes
Inflammation
Lung
Allergens
Asthma
Messenger RNA
Ovalbumin
Cytokines
T-Lymphocytes
Antigens
Proteins

All Science Journal Classification (ASJC) codes

  • General

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Increased TREM-2 expression on the subsets of CD11c+ cells in the lungs and lymph nodes during allergic airway inflammation. / Hall, Sannette C.; Agrawal, Devendra K.

In: Scientific Reports, Vol. 7, No. 1, 11853, 01.12.2017.

Research output: Contribution to journalArticle

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