Contributions from the Field
Pregnancy in patients with ankylosing spondylitis: Do regulatory T cells play a role?
Article first published online: 29 JAN 2009
Copyright © 2009 by the American College of Rheumatology
Arthritis Care & Research
Volume 61, Issue 2, pages 279–283, 15 February 2009
How to Cite
Förger, F., Villiger, P. M. and Østensen, M. (2009), Pregnancy in patients with ankylosing spondylitis: Do regulatory T cells play a role?. Arthritis & Rheumatism, 61: 279–283. doi: 10.1002/art.24161
- Issue published online: 29 JAN 2009
- Article first published online: 29 JAN 2009
- Manuscript Accepted: 19 SEP 2008
- Manuscript Received: 24 JUN 2008
- Technische Universität München HWP. Grant Number: SSZ-3/203/04
- Olga Maienfisch Fund
- Swiss National Funds. Grant Number: 320000-111936
To investigate the numerical and functional changes of CD4+CD25high regulatory T (Treg) cells during pregnancy and postpartum in patients with ankylosing spondylitis (AS).
The frequency of CD4+CD25high T cells was determined by flow cytometry in 10 pregnant and 5 nonpregnant patients with AS as well as in 14 pregnant and 4 nonpregnant healthy controls. Pregnant individuals were investigated at the third trimester and 8 weeks postpartum. Treg cells and CD4+CD25− effector T (Teff) cells separated by fluorescence-activated cell sorting were stimulated with anti-CD3 and anti-CD28 monoclonal antibodies, alone or in coculture, to investigate proliferation and cytokine secretion.
The frequency of CD4+CD25high Treg cells was significantly higher during pregnancy than postpartum in both healthy control subjects and patients with AS. In contrast to Treg cells in healthy pregnant women, Treg cells in pregnant women with AS secreted only small amounts of interleukin-10 and showed lower suppression of tumor necrosis factor α and interferon-γ secretion by CD4+CD25− Teff cells. At the postpartum time point, proinflammatory cytokine levels in the Treg/Teff cell cocultures and Teff cell monocultures were significantly higher in patients with AS than in healthy controls.
Pregnancy influenced the expansion and cytokine secretion of Treg cells in both patients with AS and control subjects. However, the Treg cells of pregnant patients with AS failed to support an antiinflammatory cytokine milieu, thereby possibly contributing to the persistent disease activity of AS during pregnancy.