PMID- 22392190
OWN - NLM
STAT- MEDLINE
DCOM- 20130104
LR  - 20240426
IS  - 1432-0851 (Electronic)
IS  - 0340-7004 (Print)
IS  - 0340-7004 (Linking)
VI  - 61
IP  - 10
DP  - 2012 Oct
TI  - Induction on differentiation and modulation of bone marrow progenitor of 
      dendritic cell by methionine enkephalin (MENK).
PG  - 1699-711
AB  - Methionine enkephalin (MENK), the endogenous neuropeptide, is known to exert 
      direct effects on the neuroendocrine and the immune systems and participates in 
      regulation of various functions of cells related to both the innate and adaptive 
      immune systems. Dendritic cells (DCs) play important role in initiating and 
      regulating T cell responses. The aim of this work is to investigate the effects 
      of MENK on differentiation, maturation, and function of DCs derived from murine 
      bone marrow progenitors (BM-derived DCs). Our result showed that MENK could 
      induce BM-derived DCs to polarize predominantly to mDC subtype, rather than pDC 
      both in vivo and in vitro, and this was in favor of Th1 response. BM-derived DCs, 
      after treatment with MENK, up-regulated the expressions of MHC class II and key 
      costimulatory molecules. Result by RT-PCR showed MENK could increase expressions 
      of delta and kappa receptors on BM-derived DCs. Also MENK promoted BM-derived DCs 
      to secret higher levels of proinflammatory cytokines of IL-12p70, TNF-alpha. 
      Furthermore, differentiated BM-derived DCs treated with MENK displayed higher 
      activity to induce allogeneic T cell proliferation and MENK also inhibited tumor 
      growth in vivo and induced apoptosis of tumor cells in vitro. Thus, it is 
      concluded that MENK could be an effective inducer of BM-derived DCs and might be 
      a new therapeutic agent for cancer, as well as other immune handicapped disease. 
      Also we may consider MENK as a potential adjuvant in vaccine preparation.
FAU - Liu, Jinling
AU  - Liu J
AD  - Department of Immunology, School of Basic Medical Science, China Medical 
      University, No. 92, North Second Road, Heping District, Shenyang 110001, People's 
      Republic of China.
FAU - Chen, Wenna
AU  - Chen W
FAU - Meng, Jingjuan
AU  - Meng J
FAU - Lu, Changlong
AU  - Lu C
FAU - Wang, Enhua
AU  - Wang E
FAU - Shan, Fengping
AU  - Shan F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120306
PL  - Germany
TA  - Cancer Immunol Immunother
JT  - Cancer immunology, immunotherapy : CII
JID - 8605732
RN  - 0 (Cytokines)
RN  - 0 (Neurotransmitter Agents)
RN  - 0 (Receptors, Opioid, delta)
RN  - 0 (Receptors, Opioid, kappa)
RN  - 58569-55-4 (Enkephalin, Methionine)
SB  - IM
EIN - Cancer Immunol Immunother. 2012 Nov;61(11):2205. Liu, Jingling [corrected to Liu, 
      Jinling]
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Bone Marrow Cells/*drug effects
MH  - Cell Differentiation/*drug effects
MH  - Cell Line, Tumor
MH  - Cytokines/metabolism
MH  - Dendritic Cells/*drug effects
MH  - Enkephalin, Methionine/*pharmacology
MH  - Female
MH  - Genes, MHC Class II/drug effects
MH  - Humans
MH  - Lymphocyte Activation/drug effects
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Neurotransmitter Agents/*pharmacology
MH  - Receptors, Opioid, delta/biosynthesis
MH  - Receptors, Opioid, kappa/biosynthesis
MH  - Stem Cells/*drug effects
MH  - Up-Regulation/drug effects
PMC - PMC11028663
COIS- The authors declare that we have no conflict of interest.
EDAT- 2012/03/07 06:00
MHDA- 2013/01/05 06:00
PMCR- 2012/03/06
CRDT- 2012/03/07 06:00
PHST- 2012/01/08 00:00 [received]
PHST- 2012/02/06 00:00 [accepted]
PHST- 2012/03/07 06:00 [entrez]
PHST- 2012/03/07 06:00 [pubmed]
PHST- 2013/01/05 06:00 [medline]
PHST- 2012/03/06 00:00 [pmc-release]
AID - 1221 [pii]
AID - 10.1007/s00262-012-1221-9 [doi]
PST - ppublish
SO  - Cancer Immunol Immunother. 2012 Oct;61(10):1699-711. doi: 
      10.1007/s00262-012-1221-9. Epub 2012 Mar 6.