About InVivoMAb hamster IgG f(ab')2 fragments The hamster IgG f(ab’)2 fragments are the f(ab’)2 fragments of polyclonal hamster IgG. The majority of the Fc fragment has been removed via pepsin digestion. This product is commonly used as a non-reactive control for the anti-mouse CD3ε F(ab’)2 fragment BE0001-1FAB. InVivoMAb hamster IgG f(ab')2 fragments Specifications IsotypePolyclonal Recommended Dilution BufferInVivoPure pH 7.0 Dilution Buffer FormulationPBS, pH 7.0 Contains no stabilizers or preservatives Endotoxin<2EU/mg (<0.002EU/μg) Determined by LAL gel clotting assay Purity>95% Determined by SDS-PAGE Sterility0.2 μm filtered ProductionPepsin Digest PurificationProtein A RRIDAB_2687680 StorageThe antibody solution should be stored at the stock concentration at 4°C. Do not freeze. Application ReferencesInVivoMAb hamster IgG f(ab')2 fragments (CLONE: hamster IgG f(ab')2 Fragments)Wilhelmson, A. S., et al (2018). "Testosterone Protects Against Atherosclerosis in Male Mice by Targeting Thymic Epithelial Cells-Brief Report" Arterioscler Thromb Vasc Biol 38(7): 1519-1527. PubMedOBJECTIVE: Androgen deprivation therapy has been associated with increased cardiovascular risk in men. Experimental studies support that testosterone protects against atherosclerosis, but the target cell remains unclear. T cells are important modulators of atherosclerosis, and deficiency of testosterone or its receptor, the AR (androgen receptor), induces a prominent increase in thymus size. Here, we tested the hypothesis that atherosclerosis induced by testosterone deficiency in male mice is T-cell dependent. Further, given the important role of the thymic epithelium for T-cell homeostasis and development, we hypothesized that depletion of the AR in thymic epithelial cells will result in increased atherosclerosis. APPROACH AND RESULTS: Prepubertal castration of male atherosclerosis-prone apoE(-/-) mice increased atherosclerotic lesion area. Depletion of T cells using an anti-CD3 antibody abolished castration-induced atherogenesis, demonstrating a role of T cells. Male mice with depletion of the AR specifically in epithelial cells (E-ARKO [epithelial cell-specific AR knockout] mice) showed increased thymus weight, comparable with that of castrated mice. E-ARKO mice on an apoE(-/-) background displayed significantly increased atherosclerosis and increased infiltration of T cells in the vascular adventitia, supporting a T-cell-driven mechanism. Consistent with a role of the thymus, E-ARKO apoE(-/-) males subjected to prepubertal thymectomy showed no atherosclerosis phenotype. CONCLUSIONS: We show that atherogenesis induced by testosterone/AR deficiency is thymus- and T-cell dependent in male mice and that the thymic epithelial cell is a likely target cell for the antiatherogenic actions of testosterone. These insights may pave the way for new therapeutic strategies for safer endocrine treatment of prostate cancer.
