Holmes K L, Schnizlein C T, Perkins E H, Tew J G
Mech Ageing Dev. 1984 Apr-May;25(1-2):243-55. doi: 10.1016/0047-6374(84)90145-3.
Our major objectives were to determine (1) when mice develop the cellular mechanisms necessary to trap and retain immune complexes in lymphoid follicles, (2) whether the ability to trap and retain immune complexes in lymphoid and collagenous tissues was maintained in old animals, and (3) whether the pattern of antigen localization in lymphoid follicles was altered as a consequence of ageing. Mice were passively immunized with a standardized amount of specific antibody and then challenged in the foot pads with radioactive antigen. The results indicated that newborn, and 1- and 2-week-old BALB/c mice lacked the cells or cellular mechanism necessary for trapping, localizing, and retaining immune complexes in lymphoid follicles. By 3 weeks, however, this ability to trap, retain, and localize antigen became apparent. The ability to trap and retain immune complexes on tendons and in lymphoid tissues was maintained as long as 27-30 months. A comparison of the quantity of antigen retained per mg of tissue in young-adult (6 months of age) and in old (27-30 months of age) mice indicated that old mice retained slightly more antigen in lymphoid tissues and substantially more on tendons. Antigen retained in spleens of both young-adult and old mice was localized in follicles by 24 h. However, the antigen retained in lymph nodes of old mice remained in the subcapsular sinus and adjacent superficial cortex and was not localized in follicles even after a full week. The cellular mechanisms necessary to trap and retain immune complexes in lymphoid tissue appear to develop in BALB/c mice a few weeks after birth and persist throughout life. However, localization of antigen in the lymphoid follicles of lymph nodes diminishes in old mice. The antigen trapping capability of collagenous tissues was not only maintained in old mice but was substantially increased.
(1)小鼠何时形成在淋巴滤泡中捕获和保留免疫复合物所需的细胞机制;(2)老龄动物在淋巴组织和胶原组织中捕获和保留免疫复合物的能力是否得以维持;(3)淋巴滤泡中抗原定位模式是否因衰老而改变。用标准化量的特异性抗体对小鼠进行被动免疫,然后在脚垫中注射放射性抗原进行激发。结果表明,新生的、1周龄和2周龄的BALB/c小鼠缺乏在淋巴滤泡中捕获、定位和保留免疫复合物所需的细胞或细胞机制。然而,到3周龄时,这种捕获、保留和定位抗原的能力变得明显。在长达27 - 30个月的时间里,肌腱和淋巴组织捕获和保留免疫复合物的能力得以维持。对年轻成年(6月龄)和老龄(27 - 30月龄)小鼠每毫克组织中保留的抗原量进行比较表明,老龄小鼠在淋巴组织中保留的抗原略多,在肌腱上保留的抗原则多得多。年轻成年小鼠和老龄小鼠脾脏中保留的抗原在24小时内定位于滤泡。然而,老龄小鼠淋巴结中保留的抗原仍留在被膜下窦和相邻的浅表皮质,即使在整整一周后也未定位于滤泡。在淋巴组织中捕获和保留免疫复合物所需的细胞机制似乎在BALB/c小鼠出生后几周内形成,并终生存在。然而,老龄小鼠淋巴结淋巴滤泡中的抗原定位减少。胶原组织的抗原捕获能力不仅在老龄小鼠中得以维持,而且显著增强。