|Title:||Tamoxifen Alleviates Disease Severity and Decreases Double Negative T Cells in Autoimmune Mrl-Lpr/Lpr Mice||Authors:||Wu, W.-M.
|Keywords:||PROTEIN-KINASE-C;SYSTEMIC LUPUS-ERYTHEMATOSUS;BREAST-CANCER CELLS;INDUCED APOPTOSIS;LPR MICE;NZBXNZW F1-MICE||Issue Date:||2000||Journal Volume:||v.100||Journal Issue:||n.1||Start page/Pages:||110-118||Source:||IMMUNOLOGY||Abstract:||
Previous study suggested that MRL-lpr/lpr mice treated with tamoxifen ( TAM) had less severe proteinuria, reduced serum titre of anti-dsDNA autoantibodies and an increased survival rate. To investigate further the regulatory mechanisms of TAM on MRL-lpr/lpr female mice, a total dose of 200 mu g per mice (5.5 mg/kg) was given every 2 weeks subcutaneously, while the control mice were injected with oil only. After being treated with TAM four times, the mice were killed and cellular functions were evaluated. The TAM-treated groups had smaller sized spleen and lymph nodes . Flow cytometric analysis of splenocytes had a significantly lower percentage of cell number of T cells and double negative T cells (CD4( -) CD8(-) T cells). There was no difference in cytokine production ( interleukin (IL)-2, IL-4, IL-5, IL-10 and interferon-gamma (IFN-gamma)) from splenocytes stimulated with concanavalin A (Con A) or cytokines (IL-6 ) secreted by peritoneal exudate cells when stimulated with lipopolysaccharide (LPS). However, IL-2 from lymph node cells was significantly higher on TAM-treated mice. Finally, splenocytes or purified T cells stimulated with anti-CD3 antibody plus cross-linking immunoglobulin G (IgG) of the TAM-treated group had higher H-3- incorporation of proliferation assay compared with that of control groups. In vitro study further demonstrated that IL-2-activated proliferation of lymph node double negative (DN) T cells can be inhibited by TAM treatment in a dose-dependent manner. Our finding demonstrated that TAM may potentially influence T cells and modulate the immune function, which offers a novel approach to explore the Feasibility of hormone therapy for autoimmune diseases.
|Appears in Collections:||醫學系|
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