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2024-05-18来源:编辑
中断的穿孔素基因的结果,在原发性免疫缺陷,并增加了敏感性,以机会主义的病原体。穿孔缺陷( pko )小鼠未能明确小学淋巴细胞choriomeningitis病毒( lcmv )阿姆斯壮,造成持续性感染及功能exhaustionof病毒特异性cd8 + t细胞。 cd8 + t细胞的反应,李斯特菌( lm )的挑战,第一个星期后lcmv感染werediminished均wtand pko小鼠,并与增强细菌清除。但是,细菌的挑战,在稍后时间点generatedsimilar cd8的tcell反应,在这两组小鼠。表型和功能的预先存在lm的特定记忆的cd8 + tcells被maintainedin坚持感染pko小鼠。因此持续lcmv感染,由于穿孔素缺乏症,结果在功能障碍的病毒- specificcd8 + t细胞的反应,但不妥协东道国的执政能力,保持原先存在的记忆cd8 + t细胞或产生新的记忆cd8 + t细胞的反应,对其他病原体。

穿孔素基因被破坏导致原发性免疫缺陷,对opportunistic病原体更敏感。穿孔素缺失的老鼠不能清理掉LCMV Armstrong,导致持续性感染和 CD8+ T细胞的功能丢失。
LCMV在WT和PKO老鼠体内的感染被清楚后一周内,CD8+ T细胞对LM产生应答反应,对细菌的清除能力增强。之后细菌的侵染在两组老鼠中都引起相同的CD8 T细胞反应。
先前LM感染后产生的CD8+记忆T细胞的表型和功能永久性存在于被感染过的小鼠中。因此,穿孔素缺失后持续性的LCMV感染导致了杀伤性T细胞的应答功能缺失,但是并没有让宿主失去原先存在的记忆性T细胞,或者说不能再产生新的记忆性T细胞来对其他的病原体做出应答反应。

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