Reed S G, Roters S B, Inverso J A, Jones T C, Goidl E A
Cell Immunol. 1985 Nov;96(1):12-25. doi: 10.1016/0008-8749(85)90336-3.
Antibody responses to T-dependent and T-"independent" antigens were studied in disease-susceptible (BALB/c and C57BL/10) and disease-resistant (A/J) mice infected with Leishmania donovani chagasi. Disease-susceptible mice but not disease-resistant mice showed a transient decrease in PFC responses to TNP on a T-dependent carrier (BGG) during the period of 4-8 weeks after infection. Infected disease-susceptible animals also showed increased responses to TNP on a type II T-independent carrier (Ficoll), which persisted until at least 14 weeks after infection. The increased responses were associated with a significant increase in anti-TNP antibody of the IgG2b subclass. When T-enriched spleen cells from infected mice and B-enriched spleen cells from uninfected mice were transferred to irradiated recipients immunized with TNP-Ficoll, increased anti-TNP PFC were observed over numbers seen in irradiated recipients which received both B and T cells from uninfected mice. Increased responses to TNP-Ficoll were also induced by prior administration of soluble leishmania extract in CFA. Infected mice immunized with TNP-LPS, a T-independent type I antigen, also had increased anti-TNP antibody responses, but had normal anti-LPS antibody responses. The elevated antibody production which occurred in response to the T-"independent" antigens could not be attributed to the relatively low polyclonal response which occurred in both disease-resistant and disease-susceptible mice infected with L. donovani chagasi. The observations are consistent with leishmania induced, transient alterations in some T-cell functions including response to haptens on T-dependent carriers, and a lack of down regulation of T-"independent" responses. Subtle lesions in immunoregulation may be important correlates of successful protozoal infection and may be responsible for some of the immunologic manifestations of the disease.
在感染杜氏利什曼原虫恰加斯亚种的疾病易感小鼠（BALB/c和C57BL/10）和疾病抗性小鼠（A/J）中，研究了对T细胞依赖性和T细胞非依赖性抗原的抗体反应。疾病易感小鼠而非疾病抗性小鼠在感染后4至8周期间，对T细胞依赖性载体（BGG）上的TNP的PFC反应出现短暂下降。受感染的疾病易感动物对II型T细胞非依赖性载体（Ficoll）上的TNP的反应也增强，这种增强至少持续到感染后14周。反应增强与IgG2b亚类抗TNP抗体的显著增加有关。当将感染小鼠的富含T细胞的脾细胞和未感染小鼠的富含B细胞的脾细胞转移到用TNP-Ficoll免疫的经照射的受体中时，观察到抗TNP PFC比接受来自未感染小鼠的B细胞和T细胞的经照射受体中的数量增加。预先在CFA中给予可溶性利什曼原虫提取物也可诱导对TNP-Ficoll的反应增强。用T细胞非依赖性I型抗原TNP-LPS免疫的感染小鼠，其抗TNP抗体反应也增强，但抗LPS抗体反应正常。对T细胞非依赖性抗原产生的抗体产生升高不能归因于感染杜氏利什曼原虫恰加斯亚种的疾病抗性和疾病易感小鼠中都出现的相对较低的多克隆反应。这些观察结果与利什曼原虫诱导的某些T细胞功能的短暂改变一致，包括对T细胞依赖性载体上半抗原的反应，以及T细胞非依赖性反应缺乏下调。免疫调节中的细微损伤可能是原生动物成功感染的重要相关因素，并且可能是该疾病某些免疫表现的原因。
