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目的：探讨伯氏疟原虫氯喹抗性与免疫的关系。方法：比较氯喹敏感株（Ｎ）和抗性株（ＲＣ）感染ＩＣＲ鼠和ＢＡＬＢ／ｃ裸鼠后的感染和再感染过程、肝脾组织学改变和血清ＩｇＧ抗体水平。结果：ＢＡＬＢ／ｃ裸鼠和ＩＣＲ鼠感染Ｎ株后，分别于４～５ｄ和７～１０ｄ死亡；大量被吞噬疟色素沉积在脾边缘区和肝脾血窦内。低剂量氯喹延长Ｎ株感染时间（３１ｄ）的ＩＣＲ鼠（ＮＣＣ），血清ＩｇＧ抗体水平增高（１∶２５６），但不能抵抗Ｎ株和ＲＣ株再感染。ＩＣＲ鼠感染ＲＣ株后，８３％在感染２８～３６ｄ自愈，自愈前脾索内淋巴细胞、浆细胞和单核－巨噬细胞不断增多；随着原虫血症迅速下降，红髓结构逐渐恢复正常，白髓生发中心形成，ＩｇＧ抗体呈强阳性（１∶４０９６）；自愈ＩＣＲ鼠能不同程度地抵制ＲＣ和Ｎ株再感染。裸鼠感染ＲＣ株４５～５６ｄ后死亡，肝脾增生浸润不明显。结论：Ｎ株引起肝脾巨噬细胞和内皮细胞的吞噬及损伤；ＲＣ株则刺激正常胸腺鼠单个核细胞增生浸润，表现为肝脾局部迟发型超敏炎症。
Objective: To investigate the relationship between chloroquine resistance and immune response of Plasmodium berghei. Methods: The infection and re-infection process, liver and spleen histological changes and serum IgG antibody levels in ICR and BALB / c nude mice infected with chloroquine-sensitive (N) and resistant (RC) strains were compared. Results: After infected with N strains of BALB / c nude mice and ICR mice, they died at 4 ~ 5d and 7 ~ 10d respectively. A large number of phagocytic malaria pigment deposition in the marginal zone of the spleen and liver and spleen sinusoids. Low doses of chloroquine prolonged the number of ICR mice (NCC) infected with N strains at the time of infection (31d), and the level of serum IgG antibody increased (1:256), but it could not resist reinfection of strains N and RC. 83% of ICR mice infected with RC strain self-healed 28-36 days after infection, and the number of lymphocytes, plasma cells and monocyte-macrophages in the splenic cord increased continually after healing. As the parasitemia decreased rapidly, the structure of red pulp gradually increased Returned to normal, the formation of white pulp germinal center, IgG antibody was strongly positive (1:4096); self-healing ICR rats to varying degrees, resisting RC and N strains reinfection. The nude mice infected with RC strain 45 ~ 56d died, infiltration of liver and spleen hyperplasia was not obvious. CONCLUSION: N strain caused phagocytosis and injury of hepatocytes and splenic macrophages and endothelial cells. RC strain stimulated proliferation and infiltration of mononuclear cells in normal thymus, which manifested as delayed-type hypersensitivity in the liver and spleen.