PMID- 29454234
OWN - NLM
STAT- MEDLINE
DCOM- 20180831
LR  - 20181202
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 56
DP  - 2018 Mar
TI  - Diarylheptanoid from rhizomes of Curcuma kwangsiensis (DCK) inhibited 
      imiquimod-induced dendritic cells activation and Th1/Th17 differentiation.
PG  - 339-348
LID - S1567-5769(18)30044-4 [pii]
LID - 10.1016/j.intimp.2018.01.044 [doi]
AB  - BACKGROUND AND OBJECT: Dendritic cells (DCs) are critical for initiating the 
      activation and differentiation of T cells in inflammatory diseases including 
      psoriasis. Curcuma kwangsiensis S.G. Lee & C.F. Liang is a herb for treating 
      psoriasis and we previously found Diarylheptanoid from rhizomes of Curcuma 
      kwangsiensis (DCK) inhibited keratinocytes proliferation. However, it is unknown 
      whether DCK influences DC functions. Thus we aimed to explore whether DCK affect 
      the major immunological functions of DCs. MATERIALS AND METHODS: Primary DCs 
      derived from mouse bone marrow cells and spleen were used for examining their 
      general immunological functions, and OVA-specific T cells from OT-II mice were 
      used for examining the DC-mediated T-helper (Th) 1 and Th17 cells differentiation 
      and effect. RESULTS: We demonstrated DCK suppressed DC uptake of FITC-labeled 
      ovalbumin (OVA) and DC maturation characterized by decreased MHCII, CD80 and CD86 
      following imiquimod (IMQ) stimulation. DCK also reduced DC expression of the 
      lymphoid-homing chemokine receptor CCR7, and DC migration towards CCL21, the 
      ligand for CCR7. Importantly, DCK significantly reduced the production of 
      proinflammatory cytokines including IL-12, IL-6 and IL-1beta by IMQ-stimulated DCs. 
      Moreover, in the coculture of OVA(323-339) peptide-pulsed DCs and OVA-specific T 
      cells from OT-II mice, DCK significantly inhibited T cell proliferation and the 
      differentiation of Th1 and Th17 cells. Furthermore, DCK treatment greatly reduced 
      phosphorylation of p65-associated cell signaling pathway in IMQ-stimulated DCs. 
      CONCLUSION: These data together demonstrate a potential role of DCK in 
      suppressing the biological function of DCs, and provide a possible mechanism for 
      understanding the effects of herb Curcuma kwangsiensis in treating psoriasis.
CI  - Copyright (c) 2018 Elsevier B.V. All rights reserved.
FAU - Liu, Qing
AU  - Liu Q
AD  - The Second Clinical School of Medicine, Guangzhou University of Chinese Medicine, 
      Guangzhou 510120, China; Department of Immunology, School of Basic Medical 
      Sciences, Fudan University, Shanghai 200030, China. Electronic address: 
      851757626@qq.com.
FAU - Yin, Wei
AU  - Yin W
AD  - Department of Immunology, School of Basic Medical Sciences, Fudan University, 
      Shanghai 200030, China.
FAU - Han, Ling
AU  - Han L
AD  - The Second Clinical School of Medicine, Guangzhou University of Chinese Medicine, 
      Guangzhou 510120, China.
FAU - Lv, Jiaoyan
AU  - Lv J
AD  - Department of Immunology, School of Basic Medical Sciences, Fudan University, 
      Shanghai 200030, China.
FAU - Li, Bingji
AU  - Li B
AD  - Department of Immunology, School of Basic Medical Sciences, Fudan University, 
      Shanghai 200030, China.
FAU - Lin, Yuli
AU  - Lin Y
AD  - Department of Immunology, School of Basic Medical Sciences, Fudan University, 
      Shanghai 200030, China.
FAU - Mi, Qingsheng
AU  - Mi Q
AD  - Henry Ford Immunology Program, Henry Ford Health System, Detroit, MI 48202, USA.
FAU - He, Rui
AU  - He R
AD  - Department of Immunology, School of Basic Medical Sciences, Fudan University, 
      Shanghai 200030, China. Electronic address: ruihe@fudan.edu.cn.
FAU - Lu, Chuanjian
AU  - Lu C
AD  - The Second Clinical School of Medicine, Guangzhou University of Chinese Medicine, 
      Guangzhou 510120, China. Electronic address: luchuanjian888@vip.sina.com.
LA  - eng
PT  - Journal Article
DEP - 20180220
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Aminoquinolines)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Diarylheptanoids)
RN  - P1QW714R7M (Imiquimod)
SB  - IM
MH  - Aminoquinolines/metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Cell Differentiation
MH  - Cells, Cultured
MH  - Curcuma/immunology
MH  - Dendritic Cells/*immunology
MH  - Diarylheptanoids/*pharmacology
MH  - Imiquimod
MH  - Lymphocyte Activation
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Rhizome
MH  - Th1 Cells/*immunology
MH  - Th17 Cells/*immunology
OTO - NOTNLM
OT  - Dendritic cell (DCs)
OT  - Diarylheptanoid from Curcuma kwangsiensis (DCK)
OT  - Psoriasis
OT  - T-helper (Th) cells
EDAT- 2018/02/18 06:00
MHDA- 2018/09/01 06:00
CRDT- 2018/02/18 06:00
PHST- 2017/10/24 00:00 [received]
PHST- 2018/01/16 00:00 [revised]
PHST- 2018/01/29 00:00 [accepted]
PHST- 2018/02/18 06:00 [pubmed]
PHST- 2018/09/01 06:00 [medline]
PHST- 2018/02/18 06:00 [entrez]
AID - S1567-5769(18)30044-4 [pii]
AID - 10.1016/j.intimp.2018.01.044 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2018 Mar;56:339-348. doi: 10.1016/j.intimp.2018.01.044. Epub 
      2018 Feb 20.