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新近研究证明 ,雌激素及其受体 (ER)参与造血和免疫功能调节。在造血干细胞、骨髓基质细胞、T细胞、B细胞和树突状细胞中都有ERα和ERβ的表达。ERα缺乏 (ERα- / - )导致胸腺和脾脏发育不全 ,不成熟的CD4 + CD8+ 双阳性细胞所占的比例增加。卵巢切除的ERβ基因敲除小鼠(ERβ- / - )给予雌激素后的表型和野生型相似 ,虽然胸腺皮层有少许退化 ,但CD4 /CD8表型没有改变。ERα- / - 小鼠骨髓细胞数稍有增加 ,而骨髓的原 /前 (pro/pre)B淋巴细胞 (B2 2 0low/IgM- )和成熟的B淋巴细胞数减少 ,而ERβ- / - 小鼠原 /前B淋巴细胞总数在骨髓和脾脏都高于野生型。ERβ- / - 小鼠还表现出髓样细胞增生性疾病 ,伴随淋巴细胞危像 ,和人慢性髓样淋巴细胞白血病相似 ,提示ERβ有抑制造血干细胞增殖和分化的作用。对ER基因多态性和自身免疫性疾病的易感性之间关系的研究 ,应因人群和疾病种类而异
Recent studies have shown that estrogen and its receptors (ER) involved in hematopoietic and immune function regulation. ERα and ERβ are expressed in hematopoietic stem cells, bone marrow stromal cells, T cells, B cells and dendritic cells. ERα deficiency (ERα- / -) leads to thymus and spleen hypoplasia, with an increased proportion of immature CD4 + CD8 + double positive cells. The phenotype after ovariectomized ERβ knockout mice (ERβ- / -) administered estrogen was similar to the wild type, with no change in the CD4 / CD8 phenotype despite a slight degeneration of the thymus. The number of myeloid cells increased slightly in ERα- / - mice, while the number of pro / pre B lymphocytes (B2 2 0low / IgM-) and mature B lymphocytes in bone marrow decreased, whereas ERβ- / - The total number of murine / pre-B-lymphocytes is higher in the bone marrow and spleen than in the wild type. ERβ- / - mice also exhibit myeloproliferative disorders with lymphocytic crisis similar to human chronic myeloid leukemia, suggesting that ERβ inhibits hematopoietic stem cell proliferation and differentiation. The relationship between ER genetic polymorphisms and susceptibility to autoimmune diseases should be based on population and disease type