PMID- 23457382
OWN - NLM
STAT- MEDLINE
DCOM- 20131029
LR  - 20131121
IS  - 1499-2752 (Electronic)
IS  - 0315-162X (Linking)
VI  - 40
IP  - 4
DP  - 2013 Apr
TI  - Effect of all-transretinoic acid on Th17 and T regulatory cell subsets in 
      patients with ankylosing spondylitis.
PG  - 476-83
LID - 10.3899/jrheum.121100 [doi]
AB  - OBJECTIVE: We compared Th17 and T regulatory cells in patients with ankylosing 
      spondylitis (AS) and in healthy controls. The effect of all-transretinoic acid 
      (ATRA) was studied on cultured CD4+ T cells of patients with AS compared to 
      controls. METHODS: Eighteen patients with AS and 18 age- and sex-matched healthy 
      controls were included. CD4+ T cells were separated and cultured in conditions of 
      anti-CD3 and anti-CD28 stimulation with and without ATRA. Intracellular and 
      secreted cytokines, transcription factors, and gene expression were evaluated 
      after 72 h. RESULTS: The frequency of CD4+IL-17+ T cells was significantly higher 
      in patients with AS compared to controls, and ATRA could significantly decrease 
      it. The frequency of forkhead box protein 3 (FOXP3)+ retinoic acid-related orphan 
      receptor gammat (RORgammat) negative T-bet negative CD4+ cells was significantly lower in 
      cases compared to controls. Intracellular and secreted interferon-gamma (IFN-gamma) was 
      not significantly different between cases and controls. ATRA significantly 
      increased intracellular IFN-gamma in cases but not in controls. Tumor necrosis 
      factor-alpha (TNF-alpha) secretion was significantly higher and interleukin 10 secretion 
      was significantly lower in culture supernatant of cases compared to controls. 
      ATRA could significantly decrease TNF-alpha secretion in cases. CONCLUSION: Our 
      findings favor a pathogenic role for Th17 cells in AS. Th1 cells did not seem to 
      contribute in the pathogenesis of this disease. The effect of ATRA as an 
      immunomodulator on deviated immune cells was associated with decreased 
      inflammatory markers. This association could be a reason for a clinical trial of 
      ATRA in patients with AS.
FAU - Bidad, Katayoon
AU  - Bidad K
AD  - Immunology, Asthma and Allergy Research Institute, Department of Immunology, 
      Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran. 
      kbidad@razi.tums.ac.ir
FAU - Salehi, Eisa
AU  - Salehi E
FAU - Jamshidi, Ahmadreza
AU  - Jamshidi A
FAU - Saboor-Yaraghi, Ali Akbar
AU  - Saboor-Yaraghi AA
FAU - Oraei, Mona
AU  - Oraei M
FAU - Meysamie, Alipasha
AU  - Meysamie A
FAU - Mahmoudi, Mahdi
AU  - Mahmoudi M
FAU - Nicknam, Mohammad Hossein
AU  - Nicknam MH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130301
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (FOXP3 protein, human)
RN  - 0 (Forkhead Transcription Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Adult
MH  - Female
MH  - Forkhead Transcription Factors/metabolism
MH  - Humans
MH  - Interleukin-10/metabolism
MH  - Male
MH  - Spondylitis, Ankylosing/*immunology/metabolism
MH  - T-Lymphocyte Subsets/*drug effects/immunology/metabolism
MH  - T-Lymphocytes, Regulatory/*drug effects/immunology/metabolism
MH  - Th17 Cells/*drug effects/immunology/metabolism
MH  - Tretinoin/*pharmacology
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2013/03/05 06:00
MHDA- 2013/10/30 06:00
CRDT- 2013/03/05 06:00
PHST- 2013/03/05 06:00 [entrez]
PHST- 2013/03/05 06:00 [pubmed]
PHST- 2013/10/30 06:00 [medline]
AID - jrheum.121100 [pii]
AID - 10.3899/jrheum.121100 [doi]
PST - ppublish
SO  - J Rheumatol. 2013 Apr;40(4):476-83. doi: 10.3899/jrheum.121100. Epub 2013 Mar 1.