Koni P A, Sacca R, Lawton P, Browning J L, Ruddle N H, Flavell R A
Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Immunity. 1997 Apr;6(4):491-500. doi: 10.1016/s1074-7613(00)80292-7.
Lymphotoxin alpha (LT alpha)-deficient mice revealed critical roles for LT alpha in lymphoid organogenesis, but it is not clear whether LT alpha functions through an LT alpha homotrimer (LT alpha3) or LT alpha/beta heterotrimers. We generated LTbeta-deficient mice and found them to lack Peyer's patches, peripheral lymph nodes, splenic germinal centers, and follicular dendritic cells. Unlike LT alpha-deficient mice, LT beta-deficient mice had cervical and mesenteric lymph nodes. Furthermore, the mesenteric lymph nodes had germinal center-like regions, although these structures appeared to lack follicular dendritic cells. The absence of cervical and mesenteric lymph nodes in LT alpha-deficient mice, and yet their presence in LT beta-deficient mice and in mice deficient in tumor necrosis factor receptor types I and II, suggest that LT alpha3 may signal via an as yet unidentified receptor.
淋巴毒素α（LTα）缺陷小鼠揭示了LTα在淋巴器官发生中的关键作用，但尚不清楚LTα是通过LTα同三聚体（LTα3）还是LTα/β异三聚体发挥作用。我们培育出了LTβ缺陷小鼠，发现它们缺乏派尔集合淋巴结、外周淋巴结、脾生发中心和滤泡树突状细胞。与LTα缺陷小鼠不同，LTβ缺陷小鼠有颈部和肠系膜淋巴结。此外，肠系膜淋巴结有类似生发中心的区域，尽管这些结构似乎缺乏滤泡树突状细胞。LTα缺陷小鼠没有颈部和肠系膜淋巴结，而LTβ缺陷小鼠以及肿瘤坏死因子受体I型和II型缺陷小鼠却有这些淋巴结，这表明LTα3可能通过一种尚未明确的受体发出信号。
