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- Title
Cigarette Smoke Extract Promotes TIM4 Expression in Murine Dendritic Cells Leading to Th2 Polarization through ERK-Dependent Pathways.
- Authors
Jiang, Rui; Jiang, Yaping; Xia, Ping; Luo, Guangwei; Huang, Wei; Hu, Zhimin; Cheng, Guilian; Xiong, Yin; Wang, Yueqin; Cui, Tianpen
- Abstract
Smoking is considered to be the main source of indoor pollution, and it has been identified as an important environmental factor contributing to asthma onset. We know that T helper 2 (Th2) response plays a crucial role in the process of asthma disease. We have investigated the reaction of cigarette smoke extract (CSE) on Th polarization which is controlled by dendritic cells (DCs). Stimulated by CSE, immature DCs from murine bone marrow showed upregulated levels of TIM4. Cocultured with CD4+ T cells, stimulated DCs increased the ratio of IL-4+ versus IFN-γ+ of CD4+ T cells. This suggests a differentiation towards Th2 response. Moreover, antibodies against TIM4 reversed the upexpression of the IL-4+/IFN-γ+ ratio provoked by CSE, indicating that the Th2 polarization which was induced by CSE is via TIM4 mechanisms. CSE could activate mitogen-activated protein kinase pathways like ERK and p38. Upregulation of TIM4 expression by CSE stimulation was found to be inhibited by an ERK inhibitor but not p38 and JNK. In conclusion, DC-induced Th2 polarization is a hallmark of CSE allergy, and this aspect can be explained by CSE-induced TIM4 expression.
- Subjects
CIGARETTE smoke; DENDRITIC cells; TH2 cells; INDOOR air pollution; BONE marrow; MITOGEN-activated protein kinases; PROTEIN kinases
- Publication
International Archives of Allergy & Immunology, 2019, Vol 178, Issue 3, p219
- ISSN
1018-2438
- Publication type
Article
- DOI
10.1159/000494505