Aichinger G, Fill H, Wick G
Lab Invest. 1985 Feb;52(2):132-40.
Surgical specimens from thyroid glands from seven patients with Hashimoto thyroiditis and two patients with non-autoimmune colloid goiter were analyzed by immunohistologic techniques (direct and indirect immunofluorescence and immunoperoxidase tests) using polyclonal antisera against total immunoglobulin, Ig classes (IgM, IgD, IgG, and IgA), and complement component C3 and monoclonal antibodies specific for B cells, T cell subpopulation, macrophages, natural killer cells, granulocytes, and HLA-DR antigen. Complement-fixing immune complexes (IgG+, C3+) were noted predominantly in areas with only slight destruction and only moderate lymphoid infiltration of thyroid follicles. In areas with intense lymphoid infiltration of thyroid follicles, where many well-developed germinal centers and significant perivascular lymphoid infiltration were seen, immune complexes were scarce. In these latter areas T helper cells (OKT4+, Leu3a+), were more abundant than T cytotoxic/suppressor cells (OKT8+), macrophages (OKM1+), and plasma cells (IgG+); only a few B lymphocytes (smIgM+, smIgD+), granulocytes (ViMD5+), and natural killer cells (VEP13+, Leu7+) were noted in the interstitium between thyroid follicles, intruding between thyroid follicular epithelial cells and merging into the thyroid follicular lumen. Many activated T cells (OKT10+, HLA-DR+) were present in these areas of advanced destruction. HLA-DR antigen expression was seen on macrophages, tissue reticulum cells, vascular endothelial cells, lymphoid cells, and, most interestingly, on thyroid epithelial cells. Normal thyroid epithelial cells did not express HLA-DR. Only a few epithelial cells in the vicinity of lymphoid infiltrations were HLA-DR+ in early stages of Hashimoto thyroiditis, and the number of HLA-DR+ epithelial cells was significantly increased in advanced stages of the disease. In our present report the potential role of HLA-DR+ thyroid epithelial cells for the in situ stimulation of the immune system within the thyroid gland of patients with Hashimoto thyroiditis is discussed, and it is hypothesized that HLA-DR+ thyroid epithelial cells may be an important factor for the progression and self-perpetuation of the disease, which is probably initiated by humoral components of the immune system but further propagated by cellular immunopathologic mechanisms.
采用抗总免疫球蛋白、Ig类别（IgM、IgD、IgG和IgA）及补体成分C3的多克隆抗血清，以及针对B细胞、T细胞亚群、巨噬细胞、自然杀伤细胞、粒细胞和HLA - DR抗原的单克隆抗体，运用免疫组织学技术（直接和间接免疫荧光及免疫过氧化物酶试验），对7例桥本甲状腺炎患者和2例非自身免疫性胶样甲状腺肿患者的甲状腺手术标本进行了分析。补体结合免疫复合物（IgG +、C3 +）主要见于甲状腺滤泡仅有轻微破坏和中度淋巴细胞浸润的区域。在甲状腺滤泡有强烈淋巴细胞浸润、可见许多发育良好的生发中心和显著血管周围淋巴细胞浸润的区域，免疫复合物较少。在这些后一类区域，辅助性T细胞（OKT4 +、Leu3a +）比细胞毒性/抑制性T细胞（OKT8 +）、巨噬细胞（OKM1 +）和浆细胞（IgG +）更为丰富；在甲状腺滤泡之间的间质中，仅发现少数B淋巴细胞（smIgM +、smIgD +）、粒细胞（ViMD5 +）和自然杀伤细胞（VEP13 +、Leu7 +），它们侵入甲状腺滤泡上皮细胞之间并融入甲状腺滤泡腔。在这些严重破坏区域存在许多活化T细胞（OKT10 +、HLA - DR +）。HLA - DR抗原表达见于巨噬细胞、组织网状细胞、血管内皮细胞、淋巴细胞，最有意思的是，也见于甲状腺上皮细胞。正常甲状腺上皮细胞不表达HLA - DR。在桥本甲状腺炎早期，仅在淋巴细胞浸润附近的少数上皮细胞为HLA - DR +，而在疾病晚期，HLA - DR +上皮细胞的数量显著增加。在本报告中，讨论了HLA - DR +甲状腺上皮细胞在桥本甲状腺炎患者甲状腺内原位刺激免疫系统的潜在作用，并推测HLA - DR +甲状腺上皮细胞可能是疾病进展和自我延续的一个重要因素，该疾病可能由免疫系统的体液成分引发，但通过细胞免疫病理机制进一步传播。
