Foltzer C, Leclercq-Meyer V, Mialhe P
Diabete Metab. 1975 Mar;1:39-44.
Recent clinical and immunological data suggest that the classical concept of "idiopathic autoimmune diseases" is to be revised. In a normal population, autoimmunity reactions against thyroid gland, gastric mucosa and adrenals develop slowly with increasing age and are found more frequently in women than in men (at least so far as thyroid antibodies are concerned) as is lowering of the functional activity of T lymphocytes. Diabetes takes its place among a series of factors diminishing immunocyte reactivity, and thus enhancing the development of the autoimmunity process. This may perhaps be promoted in some way by genetic factors, perhaps those which also play a definite though as yet ill-defined role in determining the emergence of diabetes. For the present, diabetes mellitus itself must only rarely be considered a consequence of an autoimmune process and then only in certain insulin-dependent cases. By contrast, diabetes appears frequently to be an activator of autoimmune phenomena against tissues other than pancreas, namely thyroid gland, adrenals and gastric mucosa. Awareness of these associations should encourage physicians to seek latent humoral or cellular evidence of autoimmune phenomena in diabetics; this would favour the early recognition of clinically important abnormalities which may accompany the diabetes.
最近的临床和免疫学数据表明,“特发性自身免疫性疾病”的传统概念需要修订。在正常人群中,针对甲状腺、胃黏膜和肾上腺的自身免疫反应会随着年龄的增长而缓慢发展,并且在女性中比在男性中更常见(至少就甲状腺抗体而言),T淋巴细胞功能活性的降低也是如此。糖尿病是一系列降低免疫细胞反应性从而促进自身免疫过程发展的因素之一。这可能在某种程度上受到遗传因素的推动,也许这些遗传因素在决定糖尿病的发生中也起着明确但尚未明确的作用。目前,糖尿病本身很少被认为是自身免疫过程的结果,仅在某些胰岛素依赖型病例中才会如此。相比之下,糖尿病似乎经常是针对胰腺以外组织(即甲状腺、肾上腺和胃黏膜)的自身免疫现象的激活剂。认识到这些关联应促使医生在糖尿病患者中寻找自身免疫现象的潜在体液或细胞证据;这将有助于早期识别可能伴随糖尿病出现的具有临床重要性的异常情况。