PMID- 17949549
OWN - NLM
STAT- MEDLINE
DCOM- 20080122
LR  - 20170112
IS  - 0392-856X (Print)
IS  - 0392-856X (Linking)
VI  - 25
IP  - 4 Suppl 45
DP  - 2007 Jul-Aug
TI  - Dendritic cell subsets and type I interferon system in Behcet's disease: does 
      functional abnormality in plasmacytoid dendritic cells contribute to Th1 
      polarization?
PG  - S34-40
AB  - OBJECTIVE: Several lines of evidence point to a polarized T-helper-1 (Th1) immune 
      response in Behcet's disease (BD). However, it is not yet clear which factors are 
      involved in the proposed Th1 mediated pathogenesis of BD. Dendritic cells (DCs) 
      are antigen presenting cells which play a crucial role in the polarization of 
      immune response. No previous study has examined the possible role of DCs in the 
      pathogenesis of BD. We conducted both quantitative and functional analysis of the 
      peripheral blood DC subsets in BD patients with different clinical presentations. 
      METHODS: Thirty-eight patients with BD, 12 healthy controls (HC), and 12 patients 
      with undifferentiated spondylarthritis (uSpA) were enrolled in the study. 
      Peripheral blood DC subsets were analysed by flow cytometry and were further 
      characterized for maturation with CCR7. Serum levels of interferon (IFN)-alpha 
      and IFN-b were measured by ELISA. RESULTS: BD patients had a decreased percentage 
      of plasmacytoid DCs (pDCs) compared to HC (p = 0.036). IFN-alpha levels were 
      found to be increased in BD patients as compared to HC and uSPA (p < 0.001, p = 
      0.005, respectively). BD patients had decreased levels of IFN-Beta as compared to 
      HC and uSpA (p = 0.013, p = 0.004, respectively). No difference was found between 
      HC and patients with uSpA regarding IFN-Beta levels. Subgroup analysis of BD 
      patients disclosed normalization of percentage of pDCs and the level of IFN-Beta 
      in patients receiving IFN-alpha-2b. CONCLUSION: We suggest abnormalities in pDCs 
      and type I IFNs appear to be a master switch leading to the pathogenicity in BD 
      by directing immune response towards Th1.
FAU - Pay, S
AU  - Pay S
AD  - Division of Rheumatology, Gulhane Military School of Medicine, Ankara, Turkey. 
      salihp@yahoo.com
FAU - Simsek, I
AU  - Simsek I
FAU - Erdem, H
AU  - Erdem H
FAU - Pekel, A
AU  - Pekel A
FAU - Musabak, U
AU  - Musabak U
FAU - Sengul, A
AU  - Sengul A
FAU - Dinc, A
AU  - Dinc A
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Clin Exp Rheumatol
JT  - Clinical and experimental rheumatology
JID - 8308521
RN  - 0 (Interferon-alpha)
RN  - 77238-31-4 (Interferon-beta)
SB  - IM
MH  - Adult
MH  - Behcet Syndrome/blood/*immunology/physiopathology
MH  - Case-Control Studies
MH  - Cell Communication
MH  - Dendritic Cells/*classification/*immunology/pathology
MH  - Female
MH  - Humans
MH  - Interferon-alpha/immunology
MH  - Interferon-beta/immunology
MH  - Male
MH  - Spondylarthritis/blood/immunology
MH  - Th1 Cells/*immunology/pathology
EDAT- 2007/11/14 09:00
MHDA- 2008/01/23 09:00
CRDT- 2007/11/14 09:00
PHST- 2007/11/14 09:00 [pubmed]
PHST- 2008/01/23 09:00 [medline]
PHST- 2007/11/14 09:00 [entrez]
AID - 2124 [pii]
PST - ppublish
SO  - Clin Exp Rheumatol. 2007 Jul-Aug;25(4 Suppl 45):S34-40.