Steel C, Guinea A, McCarthy J S, Ottesen E A
Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda, MD.
Lancet. 1994 Apr 9;343(8902):890-3. doi: 10.1016/s0140-6736(94)90009-4.
To identify long-term effects of prenatal exposure to maternal filarial-parasite infection, we assessed lymphocyte responses in 21 Polynesian children born 17-19 years previously to mothers diagnosed as being microfilaraemic or infection-free. All children lived on an island endemic for bancroftian filariasis but were free from infection at the time of study. While children (n = 10) of infection-free mothers responded vigorously to microfilarial antigen with lymphocyte proliferation, production of interleukin 2 (IL-2), IL-5, IL-10, granulocyte macrophage colony-stimulating factor (GM-CSF), and interferon gamma (IFN-gamma), cellular hyporesponsiveness was seen in children (n = 11) born to microfilaraemic mothers. The hyporesponsiveness appeared restricted to microfilarial antigens and did not extend to non-parasite antigens. These findings suggest that hyporesponsiveness resulted from in-utero acquisition of tolerance to microfilarial antigens in chronically-infected mothers.
为了确定产前暴露于母体丝虫寄生虫感染的长期影响,我们评估了21名波利尼西亚儿童的淋巴细胞反应,这些儿童在17至19年前出生,其母亲被诊断为微丝蚴血症或未感染。所有儿童都生活在班氏丝虫病流行的岛屿上,但在研究时未感染。未感染母亲的儿童(n = 10)对微丝蚴抗原的淋巴细胞增殖反应强烈,产生白细胞介素2(IL-2)、IL-5、IL-10、粒细胞巨噬细胞集落刺激因子(GM-CSF)和干扰素γ(IFN-γ),而微丝蚴血症母亲所生的儿童(n = 11)则出现细胞低反应性。这种低反应性似乎仅限于微丝蚴抗原,并未扩展到非寄生虫抗原。这些发现表明,低反应性是由于子宫内获得了对慢性感染母亲体内微丝蚴抗原的耐受性所致。