由抗原刺激的猫CD8(+) T淋巴细胞产生的抗猫免疫缺陷病毒（FIV）可溶性因子可抑制FIV复制。
Anti-feline immunodeficiency virus (FIV) soluble factor(s) produced from antigen-stimulated feline CD8(+) T lymphocytes suppresses FIV replication.
作者信息
Choi I S, Hokanson R, Collisson E W
机构信息
Department of Veterinary Pathobiology, Texas A&M University, College Station, Texas 77843-4467, USA.
出版信息
J Virol. 2000 Jan;74(2):676-83. doi: 10.1128/jvi.74.2.676-683.2000.
Feline immunodeficiency virus (FIV) causes AIDS-like symptoms in infected cats. Concanavalin A (ConA)-stimulated peripheral blood mononuclear cells (PBMC) from chronically FIV strain PPR-infected cats readily expressed FIV. In contrast, when PBMC from these animals were stimulated with irradiated, autologous antigen-presenting cells (APC), at least a 10-fold drop in viral production was observed. In addition to FIV-specific cytotoxic T lymphocytes, anti-FIV activity was demonstrated in the cell-free supernatants of effector T lymphocytes stimulated with APC. The FIV-suppressive activity was induced from APC-stimulated PBMC of either FIV-infected or uninfected cats but not from ConA-stimulated PBMC. Suppression of FIV strain PPR replication was observed for both autologous and heterologous feline PBMC, was dose dependent, and demonstrated cross-reactivity and cell specificity. It was also demonstrated that the anti-FIV activity originated from CD8(+) T lymphocytes and was mediated by a noncytolytic mechanism.
猫免疫缺陷病毒（FIV）在受感染的猫中引发类似艾滋病的症状。来自长期感染FIV毒株PPR的猫的伴刀豆球蛋白A（ConA）刺激的外周血单核细胞（PBMC）很容易表达FIV。相比之下，当用经辐照的自体抗原呈递细胞（APC）刺激这些动物的PBMC时，观察到病毒产生至少下降了10倍。除了FIV特异性细胞毒性T淋巴细胞外，在用APC刺激的效应T淋巴细胞的无细胞上清液中也证明了抗FIV活性。FIV抑制活性是由FIV感染或未感染猫的APC刺激的PBMC诱导产生的，而不是由ConA刺激的PBMC诱导产生的。对于自体和异源猫PBMC均观察到FIV毒株PPR复制的抑制，呈剂量依赖性，并表现出交叉反应性和细胞特异性。还证明了抗FIV活性源自CD8(+) T淋巴细胞，并由非细胞溶解机制介导。
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