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Abstract
Estrogens and estrogen receptors (ERs) are potent regulators of the immune response. Disruption of ERα or modulation of its function by selective ligands during experimental autoimmune conditions changes the course of disease by influencing specific humoral and cellular responses. However, it is not known whether fluctuation in the ERα level and the variable accessibility to its ligands in immune cells influence the development of specific immune responses against auto-antigens. This study was designed to evaluate the expression level of ERα in splenic immune cells and the specific humoral immune response in male C3H/He/W mice immunized with syngeneic testicular germ cells (TGC) in the presence of tamoxifen. Levels of ERα protein in immune cell subpopulations of immunized mice (assessed by flow cytometry) increased in MHCII+CD86+, MHCII+CD86− , F4/80+MHCII+, immature macrophages (F4/80+/MHCII− ), and CD3+CD4+ T cells. Addition of tamoxifen decreased the level of ERα in MHCII+CD86+, MHCII+CD86− , F4/80+MHCII+, immature macrophages (F4/80+/MHCII− ), and the CD19+CD3− cell subpopulation of immunized mice. Therefore, immunization with syngeneic antigen and tamoxifen treatment evoked cell-type specific changes in the level of ERα. Irrespective of tamoxifen treatment the humoral response in immunized animals toward TGCs was similar, suggesting that modulation of the level of ERα in immune cells is not directly related to specific auto-antibody production.
Declaration of interest: This work was supported by grants from the Polish Ministry of Sciences and Higher Education, grant numbers N308 009 31/3409 and POL-POSTDOC III Nr PBZ/MNiSW/07/2006/12, and by funds from the IIET. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.