RT Journal Article
SR Electronic
T1 Tumor Necrosis Factor-α Blockade Leads to Decreased Peripheral T Cell Reactivity and Increased Dendritic Cell Number in Peripheral Blood of Patients with Ankylosing Spondylitis
JF The Journal of Rheumatology
JO J Rheumatol
FD The Journal of Rheumatology
SP 2220
OP 2228
DO 10.3899/jrheum.080219
VO 35
IS 11
A1 LIPING PANG
A1 LISHA WANG
A1 TALIN SUO
A1 HUIQIN HAO
A1 XIANFENG FANG
A1 JUNYING JIA
A1 FENG HUANG
A1 JIE TANG
YR 2008
UL http://www.jrheum.org/content/35/11/2220.abstract
AB Objective To study the effect of tumor necrosis factor-α (TNF-α) antagonist (etanercept) treatment on the peripheral T cell reactivity of patients with ankylosing spondylitis (AS). Methods Peripheral blood mononuclear cells were collected from 40 patients with AS at baseline, after 2 and 6 weeks of etanercept treatment or placebo treatment, and from healthy controls. The number of cells secreting various cytokines was detected by enzyme linked immunospot. Serum soluble interleukin 2 (IL-2) receptor level was measured by ELISA. T cell proliferation was assayed with the WST-1 live cell-staining method. The myeloid dendritic cell (mDC) and regulatory T cell (Treg) levels were analyzed by fluorescence activated cell sorting. Results After 2 and 6 weeks of etanercept treatment, the number of TNF-α-secreting monocytes decreased. Although the T cell proliferation rate remained stable, the number of T cells secreting IL-2 and interferon-γ under anti-CD3/anti-CD28 stimulation was significantly decreased. The level of serum soluble IL-2R (sIL-2R), a T cell activation marker, also declined. The changes in T cell reactivity were correlated with a significant increase in MHC Class II-positive mDC cells in circulation. An increase in Treg cell numbers was also observed. Conclusion The anti-TNF-α therapy blockaded MHC Class II-positive mDC maturation, enhanced regulatory T cell levels, and suppressed the functions of effector T cells. The reduced T cell reactivity could contribute to the efficacy of the TNF-α antagonist therapy in patients with AS.