THYMIC B CELL ACTIVATION IN MYASTHENIA GRAVIS

胸腺与肌无力的发病机制有关 重症肌无力（MG），但其确切作用仍有待阐明。 几 已经描述了异常的胸腺内免疫现象。 的 传统上认为胸腺不是抗体产生的部位 但在MG中，它经常是强烈的B细胞活动的场景。 乙酰胆碱受体（AChR）抗体，是重要的致病因子， 是这种胸腺B细胞活性的产物。 此外，乙酰胆碱受体， 自身抗原在胸腺细胞上表达。 因此，有可能 自身致敏作用的发生和持续 车厢 借助于体外B细胞分化模型， 我们将研究B淋巴细胞和群体的功能特性 从MG患者胸腺获得的免疫调节细胞。 将与B淋巴细胞的特性进行比较， 免疫调节细胞：1）自体血液;和2）胸腺细胞 控制对象的暂停。 具体而言，我们将确定：1）如果 MG B淋巴细胞的异型活动反映了这些细胞的独特性质。 细胞或它们所暴露的免疫调节环境; 2） 我们发现频率增加的LA阳性细胞的同一性 在MG胸腺细胞悬液中;以及，3）如果MG胸腺含有独特的B 细胞活化剂 增加了对生物多样性机制的了解， MG患者胸腺B细胞反应增强可能会增强我们的免疫功能。 了解异常的局部胸腺内免疫事件， 可能有助于阐明负责启动，增强， 和/或疾病的延续。

The thymus gland has been implicated in the pathogenesis of myasthenia gravis (MG) but its precise role remains to be elucidated. Several aberrant intrathymic immunological phenomena have been described. The thymus is traditionally not considered to be a site of antibody production but in MG it is frequently the scene of intense B cell activity. Acetylcholine receptor (AChR) antibody, and important pathogenetic factor, is a product of this thymic B cell activity. In addition, AChR, the autoantigen, is expressed on thymic cells. Thus, there is the potential for autosensitization to occur and be perpetuated in this lymphoid compartment. With the aid of an in vitro model of B cell differentiation, we will examine the functional properties of B lymphocytes and populations of immunoregulatory cells obtained from thymuses of patients with MG. Comparisons will be made with the properties of B lymphocytes and immunoregulatory cells in: 1) autologous blood; and, 2) thymic cell suspensions of control subjects. Specifically, we will determine: 1) if anamolous activity of MG B lymphocytes reflects unique properties of these cells or the immunoregulatory milieu to which they are exposed; 2) the identity of the la-positive cells found by us to be increased in frequency in MG thymus cell suspensions; and, 3) if MG thymus contains an unique B cell activator. Increased knowledge of the mechanism underlying the augmented thymic B cell response in MG will likely enhance our understanding of aberrant local intrathymic immune events and ultimately may help to clarify mechanisms responsible for initiation, potentiation, and/or perpetuation of disease.