期刊
CELLULAR IMMUNOLOGY
卷 287, 期 1, 页码 53-61出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2013.11.007
关键词
MHC-II; Macrophage; Dendritic cells; BCG vaccine; Antigen processing; Toll-like receptor (TLR); MARCH1 ubiquitin ligase; IL-10; CD86; CD80
资金
- NIH, NIAID [AI78420, AI49534]
Tuberculosis is a major cause of death in mankind and BCG vaccine protects against childhood but not adult tuberculosis. BCG avoids lysosomal fusion in macrophages decreasing peptides required for activating CD4 T cells and Th1 immunity while suppressing the expression of MHC-II by antigen presenting cells (APCs). An in vitro model of antigen presentation showed that ligands for TLR-9, 7,4 and 1/2 increased the ability of APCs to present antigen-85B of BCG to CD4 T cells, which correlated with an increase in MHC-II expression. TLR-activation led to a down-regulation of MARCH1 ubiquitin ligase which prevents the degradation of MIC-II and decreased IL-10 also contributed to an increase in MIC-II. TLR-activation induced up-regulation of MHC-II was inhibited by the blockade of IRAK, NF-kB, and MAPKs. TLR-7 and TLR-9 ligands had the most effective adjuvant like effect on MHC-II of APCs which allowed BCG vaccine mediated activation of CD4 T cells. Published by Elsevier Inc.
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