Tolosa E, Roura C, Catálfamo M, Martí M, Lucas-Martín A, Sanmartí A, Salinas I, Obiols G, Foz-Sala M, Pujol-Borrell R
Immunology Unit, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Spain.
J Autoimmun. 1992 Feb;5(1):107-18. doi: 10.1016/s0896-8411(05)80055-1.
The presence of intercellular adhesion molecule-1 (ICAM-1) on epithelial cells facilitates their recognition by specific T lymphocytes. To assess the possible role of ICAM-1 in the recognition of thyroid follicular cells by T cells in thyroid autoimmune disease, we investigated the expression of ICAM-1 in thyrocytes from thyroid glands affected by Graves' disease, in glands with non-autoimmune pathology and normal glands using immunofluorescence staining on cryostat sections and on dispersed cell preparations. Sequential tissue sections from glands affected by Graves' disease (n = 15), multinodular goitre (MNG, n = 26), benign nodules (n = 11), primary carcinomas (n = 12) and control thyroid glands (n = 5) were stained for ICAM-1, HLA class I, HLA class II, CD3 and thyroid peroxidase (TPO). Weak and patchy ICAM-1 expression was found in the thyrocytes of 4/15 (27%) Graves' disease and of 1/26 (4%) multinodular goitre glands. In contrast, ICAM-1 expression was detected in the thyrocytes of 5/11 (45%) benign nodules and of 8/12 (67%) thyroid carcinomas in which it was sometimes strong. Thyrocytes in the five control glands were negative. These results correlated well with flow cytometry data from 23 of these glands which showed that ICAM-1 expression in thyrocytes from Graves' patients was, when present, 'dull', while in some malignant thyrocytes it was 'bright'. In preparations of thyrocytes from Graves' disease glands we found a striking discordance between the high levels of expression of HLA class I and HLA class II and the low expression of ICAM-1. This is surprising since in vitro the expression of these three molecules is equally induced by IFN-gamma and TNF-alpha. These results suggest that additional factors are involved in the induction of the inappropriate HLA class II expression observed in the thyrocytes of glands affected by Graves' disease.
上皮细胞上细胞间黏附分子-1（ICAM-1）的存在有助于其被特定T淋巴细胞识别。为评估ICAM-1在甲状腺自身免疫性疾病中T细胞识别甲状腺滤泡细胞的可能作用，我们采用冷冻切片和分散细胞制剂免疫荧光染色法，研究了格雷夫斯病（Graves' disease）患者受累甲状腺、非自身免疫性病理改变的腺体以及正常腺体中甲状腺细胞ICAM-1的表达情况。对格雷夫斯病（n = 15）、多结节性甲状腺肿（MNG，n = 26）、良性结节（n = 11）、原发性癌（n = 12）和对照甲状腺腺体（n = 5）的连续组织切片进行ICAM-1、HLA I类、HLA II类、CD3和甲状腺过氧化物酶（TPO）染色。在4/15（27%）的格雷夫斯病患者和1/26（4%）的多结节性甲状腺肿腺体的甲状腺细胞中发现ICAM-1表达微弱且呈斑片状。相比之下，在5/11（45%）的良性结节和8/12（67%）的甲状腺癌的甲状腺细胞中检测到ICAM-1表达，且有时表达较强。五个对照腺体中的甲状腺细胞呈阴性。这些结果与其中23个腺体的流式细胞术数据高度相关，流式细胞术数据显示，格雷夫斯病患者甲状腺细胞中的ICAM-1表达若存在则“暗淡”，而在一些恶性甲状腺细胞中则“明亮”。在格雷夫斯病腺体的甲状腺细胞制剂中，我们发现HLA I类和HLA II类的高表达水平与ICAM-1的低表达之间存在明显差异。这很令人惊讶，因为在体外，这三种分子的表达均由γ干扰素和肿瘤坏死因子-α同等诱导。这些结果表明，在格雷夫斯病患者受累腺体的甲状腺细胞中观察到的不适当HLA II类表达的诱导涉及其他因素。
