PMID- 17015715
OWN - NLM
STAT- MEDLINE
DCOM- 20070206
LR  - 20190516
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 177
IP  - 8
DP  - 2006 Oct 15
TI  - Suppression of experimental autoimmune myasthenia gravis by 
      granulocyte-macrophage colony-stimulating factor is associated with an expansion 
      of FoxP3+ regulatory T cells.
PG  - 5296-306
AB  - Dendritic cells (DCs) have the potential to activate or tolerize T cells in an 
      Ag-specific manner. Although the precise mechanism that determines whether DCs 
      exhibit tolerogenic or immunogenic functions has not been precisely elucidated, 
      growing evidence suggests that DC function is largely dependent on 
      differentiation status, which can be manipulated using various growth factors. In 
      this study, we investigated the effects of mobilization of specific DC 
      subsets-using GM-CSF and fms-like tyrosine kinase receptor 3-ligand (Flt3-L)-on 
      the susceptibility to induction of experimental autoimmune myasthenia gravis 
      (EAMG). We administered GM-CSF or Flt3-L to C57BL/6 mice before immunization with 
      acetylcholine receptor (AChR) and observed the effect on the frequency and 
      severity of EAMG development. Compared with AChR-immunized controls, mice treated 
      with Flt3-L before immunization developed EAMG at an accelerated pace initially, 
      but disease frequency and severity was comparable at the end of the observation 
      period. In contrast, GM-CSF administered before immunization exerted a sustained 
      suppressive effect against the induction of EAMG. This suppression was associated 
      with lowered serum autoantibody levels, reduced T cell proliferative responses to 
      AChR, and an expansion in the population of FoxP3+ regulatory T cells. These 
      results highlight the potential of manipulating DCs to expand regulatory T cells 
      for the control of autoimmune diseases such as MG.
FAU - Sheng, Jian Rong
AU  - Sheng JR
AD  - Department of Neurology and Rehabilitation, University of Illinois, Chicago, IL 
      60612, USA.
FAU - Li, Liangcheng
AU  - Li L
FAU - Ganesh, Balaji B
AU  - Ganesh BB
FAU - Vasu, Chenthamarakshan
AU  - Vasu C
FAU - Prabhakar, Bellur S
AU  - Prabhakar BS
FAU - Meriggioli, Matthew N
AU  - Meriggioli MN
LA  - eng
GR  - 1R01AI058290-01/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Forkhead Transcription Factors)
RN  - 0 (Foxp3 protein, mouse)
RN  - 0 (Membrane Proteins)
RN  - 0 (Receptors, Cholinergic)
RN  - 0 (flt3 ligand protein)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Animals
MH  - Autoimmune Diseases/therapy
MH  - Cell Communication/immunology
MH  - Cell Proliferation/*drug effects
MH  - Dendritic Cells/drug effects/immunology
MH  - *Forkhead Transcription Factors
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/administration & 
      dosage/*pharmacology
MH  - Immunization
MH  - Membrane Proteins/administration & dosage/pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Myasthenia Gravis, Autoimmune, Experimental/immunology/*prevention & 
      control/therapy
MH  - Receptors, Cholinergic/administration & dosage/immunology
MH  - T-Lymphocytes, Regulatory/*cytology
EDAT- 2006/10/04 09:00
MHDA- 2007/02/07 09:00
CRDT- 2006/10/04 09:00
PHST- 2006/10/04 09:00 [pubmed]
PHST- 2007/02/07 09:00 [medline]
PHST- 2006/10/04 09:00 [entrez]
AID - 177/8/5296 [pii]
AID - 10.4049/jimmunol.177.8.5296 [doi]
PST - ppublish
SO  - J Immunol. 2006 Oct 15;177(8):5296-306. doi: 10.4049/jimmunol.177.8.5296.