Czuprynski C J, Brown J F, Young K M, Cooley A J
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison 53706.
Infect Immun. 1989 Jan;57(1):100-9. doi: 10.1128/iai.57.1.100-109.1989.
Anti-L3T4 monoclonal antibody (GK1.5) treatment significantly impaired the antilisteria resistance of mice as manifested by increased recovery of listeriae from the spleens and livers of anti-L3T4-treated mice and by greater severity of damage to the liver and other organs. Anti-L3T4-treated mice demonstrated a profound decrease in their T cell-mediated responses to Listeria monocytogenes and its products; they failed to develop delayed type hypersensitivity to soluble listeria antigens in vivo, and their spleen cells proliferated poorly in response to stimulation by either mitogens or listeria antigens in vitro. Spleen cells from control listeria-infected mice produced significant amounts of gamma interferon when stimulated with listeria antigens in vitro, whereas under the same conditions spleen cells from anti-L3T4-treated listeria-infected mice failed to produce detectable gamma interferon. Anti-L3T4 treatment resulted in a slight increase in serum colony-stimulating activity as compared with control listeria-infected mice, probably as a result of the increased bacterial burden in these animals. Despite the dramatic decrease in T-cell activities, anti-L3T4-treated mice succeeded in clearing L. monocytogenes from the spleen and liver in a manner that was only slightly delayed as compared with control listeria-infected mice. In addition, anti-L3T4-treated listeria-immunized mice exhibited a moderate degree of enhanced resistance to rechallenge with L. monocytogenes, and their spleen cells were able to transfer a limited degree of antilisteria resistance to naive recipient mice. Both of these responses, however, were diminished as compared with those of control listeria-immunized mice in the same experiments. Although these observations establish a critical role for L3T4+ cells in the development of maximal resistance to listeriosis, they also suggest that compensatory mechanisms may allow mice to develop considerable antilisteria resistance even when L3T4+ cell activities are substantially reduced.
抗L3T4单克隆抗体（GK1.5）治疗显著损害了小鼠的抗李斯特菌能力，表现为抗L3T4治疗小鼠的脾脏和肝脏中李斯特菌的回收率增加，以及肝脏和其他器官的损伤更严重。抗L3T4治疗的小鼠对单核细胞增生李斯特菌及其产物的T细胞介导反应显著降低；它们在体内对可溶性李斯特菌抗原未能产生迟发型超敏反应，并且其脾细胞在体外受到丝裂原或李斯特菌抗原刺激时增殖能力较差。来自对照李斯特菌感染小鼠的脾细胞在体外受到李斯特菌抗原刺激时产生大量γ干扰素，而在相同条件下，来自抗L3T4治疗的李斯特菌感染小鼠的脾细胞未能产生可检测到的γ干扰素。与对照李斯特菌感染小鼠相比，抗L3T4治疗导致血清集落刺激活性略有增加，这可能是由于这些动物体内细菌负荷增加所致。尽管T细胞活性显著降低，但抗L3T4治疗的小鼠成功地从脾脏和肝脏中清除了单核细胞增生李斯特菌，与对照李斯特菌感染小鼠相比，清除过程仅略有延迟。此外，抗L3T4治疗的经李斯特菌免疫的小鼠对再次感染单核细胞增生李斯特菌表现出中度增强的抵抗力，并且其脾细胞能够将有限程度的抗李斯特菌能力转移给未免疫的受体小鼠。然而，在相同实验中，与对照李斯特菌免疫的小鼠相比，这两种反应均有所减弱。尽管这些观察结果确立了L3T4 +细胞在对李斯特菌病产生最大抵抗力过程中的关键作用，但它们也表明，即使L3T4 +细胞活性大幅降低，代偿机制可能仍使小鼠产生相当程度的抗李斯特菌能力。
