In situ immune complexes, lymphocyte subpopulations, and HLA-DR-positive epithelial cells in Hashimoto thyroiditis.
In situ immune complexes, lymphocyte subpopulations, and HLA-DR-positive epithelial cells in Hashimoto thyroiditis.
复制标题
桥本甲状腺炎的原位免疫复合物、淋巴细胞亚群和 HLA-DR 阳性上皮细胞。
DOI：
--
复制
发表时间：
1985
期刊：
影响因子：
--
通讯作者：
G. Wick
中科院分区：
文献类型：
--
作者：
G. Aichinger;H. Fill;G. Wick
采用免疫组织学技术（直接和间接免疫荧光和免疫过氧化物酶试验）对7例桥本甲状腺炎患者和2例非自身免疫性胶质性甲状腺肿患者的甲状腺手术标本进行分析，使用抗总免疫球蛋白、IgG类（IgM、IgD、IgG和IgA）、补体成分C3和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。补体固定免疫复合物（IgG+, C3+）主要出现在甲状腺滤泡轻度破坏和中度淋巴浸润的区域。在甲状腺滤泡淋巴浸润强烈的区域，有许多发育良好的生发中心和明显的血管周围淋巴浸润，免疫复合物很少。在后一区域，T辅助细胞（OKT4+, Leu3a+）比T细胞毒性/抑制细胞（OKT8+），巨噬细胞（OKM1+）和浆细胞（IgG+）更丰富；甲状腺滤泡间质中仅有少量B淋巴细胞（smIgM+、smIgD+）、粒细胞（ViMD5+）和自然杀伤细胞（VEP13+、Leu7+）侵入甲状腺滤泡上皮细胞之间，并融入甲状腺滤泡腔内。许多活化的T细胞（OKT10+, HLA-DR+）存在于这些晚期破坏区域。HLA-DR抗原在巨噬细胞、组织网细胞、血管内皮细胞、淋巴样细胞中表达，最有趣的是在甲状腺上皮细胞中表达。正常甲状腺上皮细胞不表达HLA-DR。桥本甲状腺炎早期淋巴浸润附近仅有少数上皮细胞为HLA-DR+，晚期HLA-DR+上皮细胞数量显著增加。在本报告中，我们讨论了HLA-DR+甲状腺上皮细胞在桥本甲状腺炎患者甲状腺内对免疫系统的原位刺激的潜在作用，并假设HLA-DR+甲状腺上皮细胞可能是疾病进展和自我延续的重要因素，这可能是由免疫系统的体液成分引发的，但进一步通过细胞免疫病理机制传播。
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.