PMID- 29312287
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 1664-3224 (Print)
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 8
DP  - 2017
TI  - Invariant Natural Killer T Cells Ameliorate Monosodium Urate Crystal-Induced 
      Gouty Inflammation in Mice.
PG  - 1710
LID - 10.3389/fimmu.2017.01710 [doi]
LID - 1710
AB  - Gout is an inflammatory arthritis caused by deposition of intra-articular 
      monosodium urate (MSU) crystal. Previous studies have focused on resident 
      macrophage, infiltrating monocyte, and neutrophil responses to MSU crystal; yet 
      the mechanisms of cellular changes and the potential involvement of other 
      regulatory immune cells remain largely unknown. Invariant natural killer T (iNKT) 
      cells, an innate type of T cell, are involved in the development of various 
      inflammatory diseases. Here, we investigate the role of iNKT cells in MSU 
      crystal-induced gouty inflammation. MSU crystal-induced inflammatory profiles in 
      an air-pouch model were examined in iNKT-deficient CD1d knockout (KO) and 
      wild-type (WT) control mice. To explore potential mechanisms of iNKT cell 
      regulation of gouty inflammation, we cocultured CD4(+) or CD4(-)iNKT cells with 
      bone marrow-derived macrophages (BMDMs). We found that iNKT cells quickly 
      migrated to the site of inflammation upon MSU crystal stimulation in WT mice. The 
      total number of infiltrating cells in CD1d KO mice, especially neutrophils, was 
      dramatically increased at 6 and 12 h (P < 0.01) post-MSU crystal challenge, 
      compared with WT controls. BMDMs cocultured with CD4(+)iNKT cells produced less 
      tumor necrosis factor-alpha and expressed higher levels of M2 macrophage markers, 
      including Clec7a, Pdcd1Ig2, and interleukin-4 (P < 0.01), compared with BMDMs 
      cocultured with CD4(-)iNKT cells or conventional CD4(+) T cells. CD4(+)iNKT cells 
      are one of the key regulators of MSU crystal-induced gouty inflammation through 
      the control of macrophage polarization. iNKT cells may serve as a new therapeutic 
      target for gout.
FAU - Wang, Jie
AU  - Wang J
AD  - Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao, 
      China.
AD  - Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health 
      System, Detroit, MI, United States.
AD  - Center for Cutaneous Biology and Immunology Research, Department of Dermatology, 
      Henry Ford Health System, Detroit, MI, United States.
FAU - Yang, Qibin
AU  - Yang Q
AD  - Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health 
      System, Detroit, MI, United States.
AD  - Center for Cutaneous Biology and Immunology Research, Department of Dermatology, 
      Henry Ford Health System, Detroit, MI, United States.
AD  - Department of Rheumatology, Affiliated Hospital of North Sichuan Medical College, 
      Nanchong, China.
FAU - Zhang, Quanbo
AU  - Zhang Q
AD  - Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health 
      System, Detroit, MI, United States.
AD  - Center for Cutaneous Biology and Immunology Research, Department of Dermatology, 
      Henry Ford Health System, Detroit, MI, United States.
AD  - Department of Gerontology, Affiliated Hospital of North Sichuan Medical College, 
      Nanchong, China.
FAU - Yin, Congcong
AU  - Yin C
AD  - Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health 
      System, Detroit, MI, United States.
AD  - Center for Cutaneous Biology and Immunology Research, Department of Dermatology, 
      Henry Ford Health System, Detroit, MI, United States.
FAU - Zhou, Li
AU  - Zhou L
AD  - Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health 
      System, Detroit, MI, United States.
AD  - Center for Cutaneous Biology and Immunology Research, Department of Dermatology, 
      Henry Ford Health System, Detroit, MI, United States.
AD  - Department of Internal Medicine, Henry Ford Health System, Detroit, MI, United 
      States.
FAU - Zhou, Jingguo
AU  - Zhou J
AD  - Department of Rheumatology, Affiliated Hospital of North Sichuan Medical College, 
      Nanchong, China.
FAU - Wang, Yangang
AU  - Wang Y
AD  - Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao, 
      China.
FAU - Mi, Qing-Sheng
AU  - Mi QS
AD  - Immunology Research Program, Henry Ford Cancer Institute, Henry Ford Health 
      System, Detroit, MI, United States.
AD  - Center for Cutaneous Biology and Immunology Research, Department of Dermatology, 
      Henry Ford Health System, Detroit, MI, United States.
AD  - Department of Internal Medicine, Henry Ford Health System, Detroit, MI, United 
      States.
LA  - eng
GR  - R01 AI119041/AI/NIAID NIH HHS/United States
PT  - Journal Article
DEP - 20171212
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
PMC - PMC5733058
OTO - NOTNLM
OT  - gout
OT  - invariant natural killer T cells
OT  - macrophage
OT  - polarization
OT  - tumor necrosis factor-alpha
EDAT- 2018/01/10 06:00
MHDA- 2018/01/10 06:01
PMCR- 2017/01/01
CRDT- 2018/01/10 06:00
PHST- 2017/09/15 00:00 [received]
PHST- 2017/11/20 00:00 [accepted]
PHST- 2018/01/10 06:00 [entrez]
PHST- 2018/01/10 06:00 [pubmed]
PHST- 2018/01/10 06:01 [medline]
PHST- 2017/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2017.01710 [doi]
PST - epublish
SO  - Front Immunol. 2017 Dec 12;8:1710. doi: 10.3389/fimmu.2017.01710. eCollection 
      2017.