PMID- 11422209
OWN - NLM
STAT- MEDLINE
DCOM- 20010712
LR  - 20190513
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 124
IP  - 2
DP  - 2001 May
TI  - Altered phenotype and function of blood dendritic cells in multiple sclerosis are 
      modulated by IFN-beta and IL-10.
PG  - 306-14
AB  - Multiple sclerosis (MS) is assumed to result from autoaggressive T cell-mediated 
      immune responses, in which T helper type 1 (Th1) cells producing cytokines, e.g. 
      IFN-gamma and lymphotoxin promote damage of oligodendrocyte-myelin units. 
      Dendritic cells (DCs) as potent antigen presenting cells initiate and orchestrate 
      immune responses. Whether phenotype and function of DCs with respect to Th1 cell 
      promotion are altered in MS, are not known. This study revealed that 
      blood-derived DCs from MS patients expressed low levels of the costimulatory 
      molecule CD86. In addition, production of IFN-gamma by blood mononuclear cells 
      (MNCs) was strongly enhanced by DCs derived from MS patients. IFN-beta and IL-10 
      inhibited the costimulatory capacity of DCs in mixed lymphocyte reaction (MLR) 
      and showed additive effects on suppression of IL-12 production by DCs. 
      Correspondingly, DCs pretreated with IFN-beta and IL-10 significantly suppressed 
      IFN-gamma production by MNCs. IFN-beta in vitro also upregulated CD80 and, in 
      particular, CD86 expression on DCs. In vitro, anti-CD80 antibody remarkably 
      increased, while anti-CD86 antibody inhibited DC-induced IL-4 production in MLR. 
      We conclude that DC phenotype and function are altered in MS, implying Th1-biased 
      responses with enhanced capacity to induce Th1 cytokine production. In vitro 
      modification of MS patients' DCs by IFN-beta and IL-10 could represent a novel 
      way of immunomodulation and of possible usefulness for future immunotherapy of 
      MS.
FAU - Huang, Y M
AU  - Huang YM
AD  - Neuroimmunology Unit, Division of Neurology, Huddinge University Hospital, 
      Karolinska Institute, Stockholm, Sweden. yu-min.huang@neurorec.ki.se
FAU - Stoyanova, N
AU  - Stoyanova N
FAU - Jin, Y P
AU  - Jin YP
FAU - Teleshova, N
AU  - Teleshova N
FAU - Hussien, Y
AU  - Hussien Y
FAU - Xiao, B G
AU  - Xiao BG
FAU - Fredrikson, S
AU  - Fredrikson S
FAU - Link, H
AU  - Link H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Antigens, CD)
RN  - 0 (B7-1 Antigen)
RN  - 0 (B7-2 Antigen)
RN  - 0 (CD86 protein, human)
RN  - 0 (Membrane Glycoproteins)
RN  - 130068-27-8 (Interleukin-10)
RN  - 187348-17-0 (Interleukin-12)
RN  - 207137-56-2 (Interleukin-4)
RN  - 77238-31-4 (Interferon-beta)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Adult
MH  - Antigens, CD/metabolism
MH  - B7-1 Antigen/metabolism
MH  - B7-2 Antigen
MH  - Dendritic Cells/*drug effects/immunology
MH  - Female
MH  - Humans
MH  - Interferon-beta/*pharmacology
MH  - Interferon-gamma/metabolism
MH  - Interleukin-10/*pharmacology
MH  - Interleukin-12/metabolism
MH  - Interleukin-4/metabolism
MH  - Leukocytes, Mononuclear/immunology
MH  - Lymphocyte Culture Test, Mixed
MH  - Membrane Glycoproteins/metabolism
MH  - Middle Aged
MH  - Multiple Sclerosis/*blood/immunology
MH  - Phenotype
MH  - Up-Regulation
PMC - PMC1906056
EDAT- 2001/06/26 10:00
MHDA- 2001/07/13 10:01
PMCR- 2002/05/01
CRDT- 2001/06/26 10:00
PHST- 2001/06/26 10:00 [pubmed]
PHST- 2001/07/13 10:01 [medline]
PHST- 2001/06/26 10:00 [entrez]
PHST- 2002/05/01 00:00 [pmc-release]
AID - cei1504 [pii]
AID - 10.1046/j.1365-2249.2001.01504.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2001 May;124(2):306-14. doi: 10.1046/j.1365-2249.2001.01504.x.