Aguayo J, Pérez M V, Trincado P, Wohllk N, Pineda G
Departamento de Medicina, Facultad de Medicina, Universidad de Chile.
Rev Med Chil. 1991 Aug;119(8):867-70.
The spontaneous expression of Class II molecules (HLA-DR) was studied in cultured thyrocytes obtained from patients with Graves Disease (n = 7), Hashimoto's Thyroiditis (n = 5), euthyroid nodular goiter, (n = 12), papillary carcinoma (n = 5), and laryngeal carcinoma (3 normal thyroid glands). If nodular goiters and papillary carcinoma are of autoimmune origin, as Graves Disease and Hashimoto's Thyroiditis, they should spontaneously express HLA-DR antigen on their cell surface as this has been considered one of the initial steps of autoimmunity. The study was performed using the cytotoxicity assay. Immediately after the thyroid glands were obtained, thyrocytes were labelled with 51-Cr and incubated overnight; the cells were destroyed by adding monoclonal antiHLA-DR antibody and rabbit complement. The cytotoxicity index (CI% + SD) which reflects 51-Cr release from lyzed cells was used to measure antigen expression. While Graves Disease's and Hashimoto's Disease's thyrocytes expressed HLA-DR in high proportion, normal thyrocytes and thyroid cells from other diseases did so in minimal proportion (28.12 +/- 10.71 vs 2.26 +/- 2.32, p < 0.001). These findings strongly suggest that nodular goiters and papillary carcinoma are not of autoimmune origin since they are unable to express HLA-DR on their cell surface. It is postulated that HLA-DR expression is the result of the influence of T lymphocytes previously sensitized to thyroid antigens.
对取自格雷夫斯病患者(n = 7)、桥本甲状腺炎患者(n = 5)、甲状腺功能正常的结节性甲状腺肿患者(n = 12)、乳头状癌患者(n = 5)以及喉癌患者(3个正常甲状腺)的培养甲状腺细胞中II类分子(HLA - DR)的自发表达进行了研究。如果结节性甲状腺肿和乳头状癌与格雷夫斯病和桥本甲状腺炎一样起源于自身免疫,那么它们的细胞表面应自发表达HLA - DR抗原,因为这被认为是自身免疫的初始步骤之一。该研究采用细胞毒性测定法进行。甲状腺获取后立即用51 - Cr标记甲状腺细胞并孵育过夜;加入单克隆抗HLA - DR抗体和兔补体破坏细胞。反映从裂解细胞中释放51 - Cr的细胞毒性指数(CI% + SD)用于测量抗原表达。虽然格雷夫斯病和桥本甲状腺炎的甲状腺细胞高比例表达HLA - DR,但正常甲状腺细胞和其他疾病的甲状腺细胞表达比例极低(28.12 +/- 10.71对2.26 +/- 2.32,p < 0.001)。这些发现强烈表明结节性甲状腺肿和乳头状癌并非起源于自身免疫,因为它们无法在细胞表面表达HLA - DR。据推测,HLA - DR表达是先前对甲状腺抗原致敏的T淋巴细胞影响的结果。