PMID- 21200384
OWN - NLM
STAT- MEDLINE
DCOM- 20110627
LR  - 20240323
IS  - 2042-0226 (Electronic)
IS  - 1672-7681 (Print)
IS  - 1672-7681 (Linking)
VI  - 8
IP  - 1
DP  - 2011 Jan
TI  - Estrogen enhances the functions of CD4(+)CD25(+)Foxp3(+) regulatory T cells that 
      suppress osteoclast differentiation and bone resorption in vitro.
PG  - 50-8
LID - 10.1038/cmi.2010.54 [doi]
AB  - Cross-talk has been shown to occur between the immune system and bone metabolism 
      pathways. In the present study, we investigated the impact of 
      CD4(+)CD25(+)Foxp3(+) regulatory T (Treg) cells on osteoclastogenesis and bone 
      resorption. Treg cells that were isolated and purified from peripheral blood 
      mononuclear cells (PBMCs) of healthy adults inhibited both the differentiation of 
      osteoclasts (OCs) from human embryo bone marrow cells (BMCs) and the pit 
      formation in a dose-dependent manner. In cell cocultures, the production levels 
      of both interleukin-10 (IL-10) and transforming growth factor-beta 1 (TGF-beta1) 
      were proportionally upregulated as the ratio of Treg cells to BMCs was increased, 
      and the inhibition of OC differentiation and bone resorption by Treg cells was 
      completely reversed by anti-IL-10 and anti-TGF-beta1 antibodies. Treatment of BMC 
      and Treg cell cocultures with 17beta-estradiol (E2) at concentrations between 10(-)(7) 
      and 10(-)(9) mol/l suppressed OC differentiation and bone resorption more efficiently 
      than it did in cultures of BMCs alone; this enhanced suppression occurred via the 
      stimulation of Treg cell IL-10 and TGF-beta1 expression. These data suggest that 
      Treg cells suppress OC differentiation and bone resorption by secreting IL-10 and 
      TGF-beta1. E2 enhances the suppressive effects of Treg cells on OC differentiation 
      and bone resorption by stimulating IL-10 and TGF-beta1 secretion from these cells. 
      Therefore, Treg cell-derived IL-10 and TGF-beta1 are likely involved in the 
      regulation of E2 on bone metabolism and represent potential therapeutic targets 
      for the treatment of postmenopausal osteoporosis (PMO).
FAU - Luo, C Y
AU  - Luo CY
AD  - Laboratory for Reproductive Immunology, Hospital and Institute of Obstetrics and 
      Gynecology, Fudan University Shanghai Medical College, Shanghai, China.
FAU - Wang, L
AU  - Wang L
FAU - Sun, C
AU  - Sun C
FAU - Li, D J
AU  - Li DJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101206
PL  - China
TA  - Cell Mol Immunol
JT  - Cellular & molecular immunology
JID - 101242872
RN  - 0 (Antigens, CD)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 130068-27-8 (Interleukin-10)
RN  - 4TI98Z838E (Estradiol)
SB  - IM
MH  - Adult
MH  - Antigens, CD/immunology
MH  - Bone Marrow Cells/cytology/drug effects/physiology
MH  - *Bone Resorption/metabolism
MH  - Cell Differentiation/immunology/physiology
MH  - Coculture Techniques
MH  - Dose-Response Relationship, Drug
MH  - Embryo, Mammalian
MH  - *Estradiol/pharmacology
MH  - Female
MH  - Humans
MH  - *Interleukin-10/immunology/metabolism
MH  - Osteoclasts
MH  - Osteoporosis, Postmenopausal/prevention & control/therapy
MH  - Receptor Cross-Talk/immunology/physiology
MH  - *T-Lymphocytes, Regulatory/cytology/immunology/metabolism
MH  - *Transforming Growth Factor beta1/immunology/metabolism
PMC - PMC4002989
EDAT- 2011/01/05 06:00
MHDA- 2011/06/28 06:00
PMCR- 2011/01/01
CRDT- 2011/01/05 06:00
PHST- 2011/01/05 06:00 [entrez]
PHST- 2011/01/05 06:00 [pubmed]
PHST- 2011/06/28 06:00 [medline]
PHST- 2011/01/01 00:00 [pmc-release]
AID - cmi201054 [pii]
AID - 10.1038/cmi.2010.54 [doi]
PST - ppublish
SO  - Cell Mol Immunol. 2011 Jan;8(1):50-8. doi: 10.1038/cmi.2010.54. Epub 2010 Dec 6.