4.5 Article

Enhanced expression of PD-L1 and IFN-γ on dendritic cells is associated with BCG-induced Th2 inhibition

期刊

CYTOKINE
卷 99, 期 -, 页码 163-172

出版社

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2017.09.005

关键词

Asthma; OVA-induced airway inflammation; Mycobacterium bovis BCG; Dendritic cells; Toll-like receptors; PD-L1

资金

  1. grants of Conselho Nacional de Desenvolvimento Cientifico e Tecnologico - CNPq [306768/2015-1, 401332/2014-4]
  2. Fundacao de Amparo a Pesquisa do Estado de Minas Gerais - FAPEMIG [APQ 00535/12, 00269/14, CDS-RED-00013-14]
  3. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)

向作者/读者索取更多资源

Accumulating evidence indicates that the exposure to Mycobacterium bovis bacillus Calmette-Guerin (BCG) prevents the development of allergy and the airway dendritic cells (DCs) may be involved in this protective effect. However, studies to better characterize the specific interactions between BCG and DCs and their role in this mycobacteria-mediated Th2 cell suppression are still ongoing. This study aimed to evaluate the effect of the neonatal BCG vaccination in the innate immune response in a mouse model of ovalbumin (OVA)-induced airway inflammation. BCG treated neonatal BALB/c mice were sensitized and challenged with aerosolized OVA. Twenty-four hours after the last challenge, samples were collected for analysis. The intranasal BCG treatment inhibited the allergic Th2-response by decreasing the allergen-induced eosinophilic inflammation, EPO activity, CCL11, IL-25, TSLP, IL-4 and IL-5 lung levels, and serum levels of IgE. Mycobacteria treatment increased lung levels of IL-10 and TGF-beta, and the TLR2 and TLR4 expressions by pulmonary CD11c(+)CD103(+)CD8 alpha(+) DCs. Additionally an enhanced expression of PD-L1 was observed besides an increased production of IFN-gamma by these cells. These results indicated that neonatal BCG vaccination inhibits key features of allergic airway inflammation, probably by promoting T regulatory immune response via an enhanced expression of TLR2, TLR4 and PD-L1 on DCs.

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