Grody W W, Fligiel S, Naeim F
Am J Clin Pathol. 1985 Jul;84(1):85-95. doi: 10.1093/ajcp/84.1.85.
Acquired immunodeficiency syndrome (AIDS) is a severe disorder of unknown etiology and pathogenesis, predominantly affecting homosexual males and other high-risk groups and characterized by profound alterations in T-lymphocyte function. The authors have examined thymus tissue from 14 patients who died of AIDS and compared the results with findings in five control groups: healthy age-matched controls, elderly individuals, patients with chronic or debilitating illnesses other than AIDS, infants with conditions causing "stress atrophy," and patients with myasthenia gravis. The AIDS group included 11 homosexual males, 1 Haitian, 1 homosexual who was also a drug abuser, and a 10-month-old infant believed to have contracted AIDS following blood transfusion. All the AIDS cases showed marked thymus involution with severe depletion of both lymphocytes and epithelial elements. The latter component consisted primarily of thin cords and nests of primitive-appearing epithelial cells that could be defined by positive immunohistochemical staining for keratin. Many cases showed a variable plasma cell infiltration, and the majority exhibited distinct vascular changes in the form of hyalinization and/or onion-skin patterns, primarily in the adventitia. Most striking of all was the marked paucity of Hassall's corpuscles; four patients had none at all, while in the other ten patients all the Hassall's corpuscles were calcified. These changes were far more extensive than those seen in any of the control groups, which retained most of their complement of Hassall's corpuscles even in the face of marked overall involution. The physiologic function of Hassall's corpuscles is not known, but recent immunohistochemical studies have implicated them in the synthesis of "facteur thymique serique" (FTS, thymulin) and other thymic hormones known to play a role in regulating T-helper and suppressor cell activity. It is conceivable that the extensive destruction of Hassall's corpuscles observed in AIDS may be a crucial element in the pathogenesis of this syndrome.
获得性免疫缺陷综合征(艾滋病)是一种病因和发病机制不明的严重疾病,主要影响同性恋男性和其他高危人群,其特征是T淋巴细胞功能发生深刻改变。作者检查了14例死于艾滋病患者的胸腺组织,并将结果与五个对照组的发现进行了比较:年龄匹配的健康对照组、老年人、除艾滋病外患有慢性或衰弱性疾病的患者、患有导致“应激性萎缩”疾病的婴儿以及重症肌无力患者。艾滋病组包括11名同性恋男性、1名海地人、1名既是同性恋又是药物滥用者的人以及一名据信因输血感染艾滋病的10个月大婴儿。所有艾滋病病例均显示胸腺明显萎缩,淋巴细胞和上皮成分严重减少。后者主要由细索状和巢状外观原始的上皮细胞组成,可通过角蛋白免疫组化染色阳性来界定。许多病例有不同程度的浆细胞浸润,大多数病例表现出明显的血管变化,形式为玻璃样变和/或洋葱皮样模式,主要在外膜。最引人注目的是哈氏小体明显稀少;4例患者完全没有哈氏小体,而在其他10例患者中,所有哈氏小体均已钙化。这些变化比任何对照组所见的变化都要广泛得多,即使在总体明显萎缩的情况下,对照组仍保留了大部分哈氏小体。哈氏小体的生理功能尚不清楚,但最近的免疫组化研究表明它们参与了“胸腺血清因子”(FTS,胸腺素)和其他已知在调节辅助性T细胞和抑制性T细胞活性中起作用的胸腺激素的合成。可以想象,在艾滋病中观察到的哈氏小体的广泛破坏可能是该综合征发病机制中的一个关键因素。