Iarilin A A, Sharova N I, Kuz'menok O I, Mitin A N, Nikonova M F, Litvina M M
Radiats Biol Radioecol. 1996 Jul-Aug;36(4):587-600.
The hypothesis is formulated, which explains genesis of long-lasting disturbances in the immune system of the persons affected by factors of Chernobyl disaster. Immunological alterations which are displayed at the late time after action of radiation in doses 0.5 Gy or lower are not a result of direct damage of the cells of immune system by irradiation. Their development is more probably a result of appearance of some systemic conditions and factors in affected organism--such as hormonal disbalance and especially autoantibodies of different specificities, including those reactive with thymic epithelial cells. Autoantibodies of the last type induce the decrease of thymic hormone secretion which results in functional deficiency of T lymphocytes. This chain of events is similar to those occurring in aging and does not directly causes development of the clinical displays of immunodeficiency. Only irradiation in doses of 4-6 Gy or higher inducing the structural damage of thymic microenvironment can rouse the long-lasting T cell immunodeficiency with the clinical manifestations.
该假说得以提出,其解释了受切尔诺贝利灾难因素影响人群免疫系统长期紊乱的成因。在0.5戈瑞或更低剂量辐射作用后的晚期出现的免疫改变,并非免疫系统细胞受辐射直接损伤的结果。其发展更可能是受影响机体中出现某些全身性状况和因素的结果,比如激素失衡,尤其是不同特异性的自身抗体,包括与胸腺上皮细胞发生反应的自身抗体。后一种类型的自身抗体导致胸腺激素分泌减少,进而造成T淋巴细胞功能缺陷。这一系列事件与衰老过程中发生的事件相似,并不会直接引发免疫缺陷的临床症状。只有4 - 6戈瑞或更高剂量的辐射诱导胸腺微环境的结构损伤,才会引发伴有临床表现的长期T细胞免疫缺陷。