Background Thalidomide was originally used to alleviate morning sickness in pregnant women, but was banned due to severe adverse effects. Since the discovery of its anticancer and anti-inflammatory properties, it has regained research interest. However, its mechanism of action is still unknown. Therefore, we examined the effects of thalidomide on effector T (Teff) and regulatory T (Treg) cells in splenocytes of mice. Methods Splenic CD4+, CD44low, and CD62Lhigh T lymphocytes (Tnaives) isolated from C57BL/6 mice were cultured for T-cell proliferation and Treg conversion. For T-cell proliferation, naive T cells (Tnaives) were cultured for 72 hours with anti-CD3 and anti-CD28 antibodies, and carboxyfluorescein succinimidyl ester (CFSE) labeling method was used. For Treg conversion, Tnaives were cultured for 72 hours with transforming growth factor-β1 (TGF-β1) and interleukin-2 (IL-2). Naïve T cells were plated at 1.5 × 105 cells on 96-well plates with 0, 1, 10, 50, or 100 μmol/L thalidomide. All samples were analyzed by flow cytometry after staining with CFSE, APC-conjugated anti-mouse CD4, and FITC-conjugated anti-mouse FoxP3. Results Thalidomide significantly decreased the proliferation of CD4+ Teffs in a dose-dependent manner (P <.01). In contrast, conversion to CD4+FoxP3+ Tregs tended to increase by thalidomide treatment, although the increase was not statistically significant. Conclusion These findings suggest that thalidomide may have an immune modulatory effect by selectively suppressing CD4+ Teff proliferation. Further studies will be needed to elucidate the underlying signaling pathway.
|Number of pages||4|
|Publication status||Published - 2015 Apr 1|
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