ArticleBMC immunology2018
Rapid loss of early antigen-presenting activity of lymph node dendritic cells against Ag85A protein following Mycobacterium bovis BCG infection.
Article in BMC immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Activation dynamics of antigen presenting cells in vivo against Mycobacterium bovis BCG in different immunized route.BMC immunology · 2023Article
- Discrepancy in Response of Mouse Dendritic Cells against BCG: Weak Immune Effects of Plasmacytoid Dendritic Cells Compared to Classical Dendritic Cells despite the Uptake of Bacilli.Tropical medicine and infectious disease · 2023Article
- Can miRNA Indicate Risk of Illness after Continuous Exposure toInternational journal of molecular sciences · 2021Article
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundControl of Mycobacterium tuberculosis (Mtb) infection requires CD4
resultsIn the present study, we evaluated in vivo dynamics of early Ag presentation by murine lymph-node (LN) DCs in response to Mycobacterium bovis bacillus Calmette-Guérin (BCG) Ag85A protein. Results showed that the early Ag-presenting activity of murine DCs induced by M. bovis BCG Ag85A protein in vivo was transient, appearing at 4 h and being barely detectable at 72 h. The transcription levels of CIITA, MHC II and the expression of MHC II molecule on the cell surface increased following BCG infection. Moreover, BCG was found to survive within the inguinal LN DC pool, representing a continuing source of mycobacterial Ag85A protein, with which LN DCs formed Ag85A peptide-MHCII complexes in vivo.
conclusionsOur results demonstrate that a decrease in Ag85A peptide production as a result of the inhibition of Ag processing to is largely responsible for the short duration of Ag presentation by LN DCs during BCG infection in vivo.
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