Berlinger N T, Lopez C, Lipkin M, Vogel J E, Good R A
J Clin Invest. 1977 May;59(5):761-9. doi: 10.1172/JCI108697.
Cancer-free individuals from family agregates of seemingly hereditary colon carcinoma were studied to determine the nature of their cell-mediated immune capacities in miexed leukocyte culture. Members of families who demonstrated no evidence of a precancerous condition such as polyposis coli did demonstrate substantial cellular immunopathology. Of these, 44% showed a decreased responsiveness of their peripheral mononuclear cells to allogeneic stimuli, and in a number of these individuals this deficiency clearly manifested itself as an inappropriate suppression of potentially normal lymphocyte blastogenic capacities by an adherent population of mononuclear leukocytes. This in vitro defect of recognitive immunity appears to be the same type of defect that has already been described for individuals with established maligancies. The pattern of phenotypic expression of this immunopathology within these families is not inconsistent with an hereditary disorder. Individuals from families with a known hereditary somatic precancerous condition usually did not demonstrate this immunopathology. It is appropriate to speculate that the defect of recognitive immunity in the former families could be contributory to the genesis of the colon carcinoma.
对来自看似遗传性结肠癌家族聚集群体中的无癌个体进行了研究，以确定他们在混合白细胞培养中细胞介导免疫能力的性质。那些没有诸如结肠息肉病等癌前病变证据的家族成员确实表现出明显的细胞免疫病理学特征。其中，44%的个体外周单核细胞对同种异体刺激的反应性降低，并且在许多这些个体中，这种缺陷明显表现为单核白细胞的黏附群体对潜在正常淋巴细胞增殖能力的不适当抑制。这种识别免疫的体外缺陷似乎与已确诊恶性肿瘤个体中描述的缺陷类型相同。这些家族中这种免疫病理学的表型表达模式与遗传性疾病并不矛盾。来自具有已知遗传性体细胞癌前病变家族的个体通常没有表现出这种免疫病理学特征。推测前一类家族中识别免疫的缺陷可能促成了结肠癌的发生是合理的。
