Function on Peyer patch in mother to infant infection with MAIDS virus

我们发现，女佣病毒通过母婴感染会导致婴儿持续感染。长期携带后出现免疫缺陷，伴有全身淋巴结肿大和脾肿大。与婴儿不同，成年小鼠在4-5周内立即患上小鼠艾滋病。我们分析了母婴慢性感染女佣病毒的机制。我们发现婴儿来源的脾细胞对刀豆素A或抗CD3抗体的刺激反应很弱。此外，检查表明，反应性差的不是抗原提呈细胞，而是T细胞。用ELISA法检测抗CD3抗体刺激小鼠脾细胞产生的细胞因子，发现γ-干扰素和IL-2的产生剂量很低，与脾细胞的增殖作用平行。但IL-4水平与成人相当。这些事实表明，Th2在新生儿中占主导地位，而在成人中则以Th1为主。我们分析了小鼠在婴儿时期接触女佣病毒抗原对成年鼠的反应性的影响。在成年小鼠中，以Th1为主的MAIDES病毒抗原可以诱导幼稚T细胞的增殖。但是，婴儿期暴露的小鼠不能做到这一点。Th2占优势状态可能不会引起急性感染，但可能会导致持续性感染。

We have found that MAIDS virus infection through mother to infant causes persistent infection in infant. They developed immunodeficiency with general lymphadenopathy and splenomegaly after long carrier state. In contrast to infant, adult mice develop immediately murin AIDS in 4-5 weeks. We analyzed the mechanism of chronic infection in mother to infant infection in MAIDS virus. We found spleen cells derived from infant showed very weak reaction for ConcanavarineA or anti-CD3 antibody stimulation. Furthermore examination demonstrated poor reactivity owed not antigen presenting cells but T cells. The cytokine production by anti-CD3 antibody stimulation was measured by ELISA.The production dose of gamma-IFN and IL2 war very low, these were parallel to the spleen cells proliferation. But, IL4 was equal to adult. These facts show Th2 is dominant in neonate, contrast to Th1 in adult. We analyzed the effect of the reactivity to the MAIDS virus antigen on adult, when mice had been exposured to them at infant. In adult mice, being Th1 dominant, MAIDS virus antigen can induce the proliferation on naive T cells. But, exposured mice at infant period can not do. Th2 dominant state may induce not acute infection but persistent infection.