Spontaneous Endometrial Hyperplasia in the Uteri of IL-2 Receptor Beta-Chain Transgenic Mice

Abstract

We found frequent and spontaneous proliferation of glandular epithelium and dilated cysts in the uteri of interleukin-2 receptor (IL2R) beta-chain transgenic (Tg2Rbeta) mice. The aim of this study was to examine the involvement of IL2R beta-chain in the pathogenesis of endometrial hyperplasia (EH). Mouse uteri and serum were collected from Tg2Rbeta and normal littermates (NL), which were classified into three groups according to age. The incidence of EH increased in an age-dependent manner in both types of mice. However, in old age, Tg2Rbeta mice showed more serious phenotypes of EH than NL. Immunohistochemical analysis revealed specific localization of IL2R beta-chain in the glandular epithelial cells, with a correlation to the degree of EH, not only in the Tg2Rbeta uteri but also in the NL uteri. Immunoreactions of CD3 and CD25 were detected in the uteri of Tg2Rbeta but were weak in the uteri of NL, and CD25-positive cells were distributed in the endometrial stroma and myometrium in the Tg2Rbeta mice. These findings suggest that the IL2R beta-chain induces growth potential for glandular epithelial cells and an immune-privileged condition mediated by CD25+regulatory-T cells.