We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Lipocalin 2 regulates expression of MHC class I molecules in Mycobacterium tuberculosis-infected dendritic cells via ROS production.
- Authors
Choi, Ji-Ae; Cho, Soo-Na; Lee, Junghwan; Son, Sang-Hun; Nguyen, Doan Tam; Lee, Seong-Ahn; Song, Chang-Hwa
- Abstract
Background: Iron has important roles as an essential nutrient for all life forms and as an effector of the host defense mechanism against pathogenic infection. Lipocalin 2 (LCN2), an innate immune protein, plays a crucial role in iron transport and inflammation. In the present study, we examined the role of LCN2 in immune cells during Mycobacterium tuberculosis (Mtb) infection. Results: We found that infection with Mtb H37Ra induced LCN2 production in bone marrow-derived dendritic cells (BMDCs). Notably, expression of MHC class I molecules was significantly reduced in LCN2−/− BMDCs during Mtb infection. The reduced expression of MHC class I molecules was associated with the formation of a peptide loading complex through LCN2-mediated reactive oxygen species production. The reduced expression of MHC class I molecules affected CD8+ T-cell proliferation in LCN2−/− mice infected with Mtb. The difference in the population of CD8+ effector T cells might affect the survival of intracellular Mtb. We also found a reduction of the inflammation response, including serum inflammatory cytokines and lung inflammation in LCN2−/− mice, compared with wild-type mice, during Mtb infection. Conclusions: These data suggest that LCN2-mediated reactive oxygen species affects expression of MHC class I molecules in BMDCs, leading to lower levels of CD8+ effector T-cell proliferation during mycobacterial infection.
- Subjects
TUBERCULOSIS; DENDRITIC cells; MYCOBACTERIAL diseases; MYCOBACTERIUM; REACTIVE oxygen species; MYCOBACTERIUM tuberculosis; T cell receptors; MOLECULES
- Publication
Cell & Bioscience, 2021, Vol 11, Issue 1, p1
- ISSN
2045-3701
- Publication type
Article
- DOI
10.1186/s13578-021-00686-2