雌激素受体 α 基因缺失并不影响实验性自身免疫性重症肌无力的发病机制。
Genetic deficiency of estrogen receptor alpha fails to influence experimental autoimmune myasthenia gravis pathogenesis.
机构信息
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, USA.
出版信息
J Neuroimmunol. 2011 May;234(1-2):165-7. doi: 10.1016/j.jneuroim.2011.03.002. Epub 2011 Apr 8.
Autoimmune myasthenia gravis (MG) is characterized by T cell and antibody responses to muscle nicotinic acetylcholine receptor (AChR). It is well known that MG as other autoimmune diseases is more prevalent in women than men and estrogen administration enhances experimental autoimmune MG (EAMG) severity. To determine whether estrogen influences EAMG pathogenesis through estrogen receptor alpha (ERα) activation, ERα knockout (KO) and wild-type (WT) C57BL/6 mice were immunized with AChR. ERα KO mice were equally susceptible to EAMG as WT mice and exhibited comparable antibody and immunopathological responses to AChR, suggesting a lack of involvement of ERα in EAMG pathogenesis.
自身免疫性重症肌无力（MG）的特征是 T 细胞和抗体对肌肉烟碱型乙酰胆碱受体（AChR）的反应。众所周知，MG 与其他自身免疫性疾病一样，女性比男性更为常见，雌激素的应用会增强实验性自身免疫性 MG（EAMG）的严重程度。为了确定雌激素是否通过雌激素受体α（ERα）的激活影响 EAMG 的发病机制，用 AChR 对 ERα 敲除（KO）和野生型（WT）C57BL/6 小鼠进行免疫。ERα KO 小鼠与 WT 小鼠一样容易发生 EAMG，并且对 AChR 表现出相似的抗体和免疫病理学反应，这表明 ERα 不参与 EAMG 的发病机制。
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