Locksley R M, Heinzel F P, Sadick M D, Holaday B J, Gardner K D
Department of Medicine, University of California San Francisco Medical Center 94143.
Ann Inst Pasteur Immunol. 1987 Sep-Oct;138(5):744-9. doi: 10.1016/s0769-2625(87)80030-2.
BALB/c mice develop fatal illness following infection with Leishmania major despite expansion of helper L3T4+ T cells in the draining lymph nodes and spleen. Healer mice, either genetically resistant C57BL/6 or BALB/c that have been pretreated with monoclonal antibody GK 1.5, also develop expanded numbers of L3T4+ T cells at the time of healing. Lymph node cells from healer mice produce gamma-interferon in vitro and message for gamma-interferon can be recovered from the lymph nodes during healing in vivo. Conversely, cells harvested from non-healer mice during the course of infection produce minimal gamma-interferon in vitro and have little message for gamma-interferon detectable in vivo. When the same Northern blots are hybridized for IL-4, large amounts of IL-4 message are detected only in cells from non-healer mice. The data are consistent with the expansion of type 1 helper cells (Th1) during healing and type 2 helper cells (Th2) during progressive leishmania infection.
尽管感染硕大利什曼原虫后引流淋巴结和脾脏中的辅助性L3T4 + T细胞会扩增,但BALB/c小鼠仍会患上致命疾病。治愈小鼠,无论是基因抗性的C57BL/6小鼠还是经单克隆抗体GK 1.5预处理的BALB/c小鼠,在治愈时L3T4 + T细胞数量也会扩增。治愈小鼠的淋巴结细胞在体外产生γ-干扰素,并且在体内治愈过程中可从淋巴结中回收γ-干扰素的信使核糖核酸。相反,在感染过程中从未治愈小鼠采集的细胞在体外产生的γ-干扰素极少,并且在体内几乎检测不到γ-干扰素的信使核糖核酸。当相同的Northern印迹用白细胞介素-4进行杂交时,仅在未治愈小鼠的细胞中检测到大量白细胞介素-4信使核糖核酸。这些数据与治愈过程中1型辅助性细胞(Th1)的扩增以及进行性利什曼原虫感染过程中2型辅助性细胞(Th2)的扩增一致。