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Publication : Th2-type inflammation instructs inflammatory dendritic cells to induce airway hyperreactivity.

First Author  Iwata A Year  2014
Journal  Int Immunol Volume  26
Issue  2 Pages  103-14
PubMed ID  24150243 Mgi Jnum  J:207021
Mgi Id  MGI:5554312 Doi  10.1093/intimm/dxt047
Citation  Iwata A, et al. (2014) Th2-type inflammation instructs inflammatory dendritic cells to induce airway hyperreactivity. Int Immunol 26(2):103-14
abstractText  Dendritic cells (DCs) play critical roles in determining the fate of CD4(+) T cells. Among DC sub-populations, monocyte-derived inflammatory DCs (iDCs) have been shown to play an important role in the induction of adaptive immune responses under inflammatory conditions. Although previous studies have shown that DCs have an indispensable role in the induction of allergic airway inflammation and airway hyperreactivity (AHR) in murine asthma models, the precise roles of iDCs in the asthmatic responses remain largely unknown. We show here that T(h)2 cell-mediated inflammation in murine asthma models induces the expression of some markers of alternatively activated macrophage such as arginase 1 and resistin-like molecule-alpha in iDCs by a mechanism depending on the intrinsic expression of STAT6. In contrast, T(h)1 cell-mediated inflammation induces iDCs to express TNF-alpha and inducible nitric oxide synthase (iNOS), markers of TNF-alpha- and iNOS-producing DCs. Moreover, we show that iDCs under a T(h)2 environment play an important role in the induction of AHR, independently of allergic airway inflammation. Our results thus indicate the importance of iDCs in the induction of AHR as downstream effector cells in T(h)2 cell-mediated asthmatic responses.
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