PT - JOURNAL ARTICLE AU - LIPING PANG AU - LISHA WANG AU - TALIN SUO AU - HUIQIN HAO AU - XIANFENG FANG AU - JUNYING JIA AU - FENG HUANG AU - JIE TANG TI - 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 AID - 10.3899/jrheum.080219 DP - 2008 Nov 01 TA - The Journal of Rheumatology PG - 2220--2228 VI - 35 IP - 11 4099 - http://www.jrheum.org/content/35/11/2220.short 4100 - http://www.jrheum.org/content/35/11/2220.full SO - J Rheumatol2008 Nov 01; 35 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.