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Title: NLRP10 Enhances CD4+ T-Cell-Mediated IFNγ Response via Regulation of Dendritic Cell-Derived IL-12 Release
Authors: Vacca, Maurizio
Böhme, Julia
Zambetti, Lia Paola
Khameneh, Hanif Javanmard
Paleja, Bhairav S.
Laudisi, Federica
Ho, Adrian W. S.
Neo, Kurt
Leong, Keith Weng Kit
Marzuki, Mardiana
Lee, Bernett
Poidinger, Michael
Santambrogio, Laura
Tsenova, Liana
Zolezzi, Francesca
De Libero, Gennaro
Singhal, Amit
Mortellaro, Alessandra
Keywords: Mycobacterium Tuberculosis
Dendritic Cells
Issue Date: 2017
Source: Vacca, M., Böhme, J., Zambetti, L. P., Khameneh, H. J., Paleja, B. S., Laudisi, F., et al. (2017). NLRP10 Enhances CD4+ T-Cell-Mediated IFNγ Response via Regulation of Dendritic Cell-Derived IL-12 Release. Frontiers in Immunology, 8, 1462-.
Series/Report no.: Frontiers in Immunology
Abstract: NLRP10 is a nucleotide-binding oligomerization domain-like receptor that functions as an intracellular pattern recognition receptor for microbial products. Here, we generated a Nlrp10−/− mouse to delineate the role of NLRP10 in the host immune response and found that Nlrp10−/− dendritic cells (DCs) elicited sub-optimal IFNγ production by antigen-specific CD4+ T cells compared to wild-type (WT) DCs. In response to T-cell encounter, CD40 ligation or Toll-like receptor 9 stimulation, Nlrp10−/− DCs produced low levels of IL-12, due to a substantial decrease in NF-κB activation. Defective IL-12 production was also evident in vivo and affected IFNγ production by CD4+ T cells. Upon Mycobacterium tuberculosis (Mtb) infection, Nlrp10−/− mice displayed diminished T helper 1-cell responses and increased bacterial growth compared to WT mice. These data indicate that NLRP10-mediated IL-12 production by DCs is critical for IFNγ induction in T cells and contributes to promote the host defense against Mtb.
DOI: 10.3389/fimmu.2017.01462
Rights: © 2017 Vacca, Böhme, Zambetti, Khameneh, Paleja, Laudisi, Ho, Neo, Leong, Marzuki, Lee, Poidinger, Santambrogio, Tsenova, Zolezzi, De Libero, Singhal and Mortellaro. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Fulltext Permission: open
Fulltext Availability: With Fulltext
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