de Kossodo S, Grau G E, Daneva T, Pointaire P, Fossati L, Ody C, Zapf J, Piguet P F, Gaillard R C, Vassalli P
Department of Pathology, University of Geneva, Switzerland.
J Exp Med. 1992 Nov 1;176(5):1259-64. doi: 10.1084/jem.176.5.1259.
Tumor necrosis factor alpha (TNF-alpha), a major mediator of inflammation, also possesses a wide pleiotropism of actions, suggesting its involvement in physiological conditions. TNF-alpha mRNA is present in mouse embryonic tissues and also in fetal thymus and spleen. Repeated injections of a monospecific polyclonal rabbit anti-mouse TNF-alpha antibody in mice, starting either during pregnancy or at birth, led to a severe but transient growth retardation, already present at birth, reaching a 35% decrease in body weight at 3 wk, with complete recovery at 8 wk. The insulin growth factor I (IGF-I) blood levels were decreased to about 50%; growth hormone release and other endocrine functions were unaltered. A marked atrophy of the thymus, spleen, and lymph nodes was also observed, with lymphopenia and impaired development of T and B cell peripheral lymphoid structures. The pathways involving TNF-alpha in IGF-I release and early body growth are probably distinct from those by which TNF-alpha participates in early development of lymphoid tissues, where its low physiological release may contribute to enhance lymphoid cell expansion.
肿瘤坏死因子α（TNF-α）是炎症的主要介质，也具有广泛的多效性作用，提示其参与生理状况。TNF-α mRNA存在于小鼠胚胎组织以及胎儿胸腺和脾脏中。在小鼠孕期或出生时开始重复注射单特异性多克隆兔抗小鼠TNF-α抗体，会导致严重但短暂的生长迟缓，出生时即已出现，3周时体重下降35%，8周时完全恢复。胰岛素生长因子I（IGF-I）的血液水平降至约50%；生长激素释放及其他内分泌功能未改变。还观察到胸腺、脾脏和淋巴结明显萎缩，伴有淋巴细胞减少以及T和B细胞外周淋巴结构发育受损。TNF-α在IGF-I释放和早期身体生长中涉及的途径可能与TNF-α参与淋巴组织早期发育的途径不同，在淋巴组织早期发育中其低水平的生理性释放可能有助于促进淋巴细胞扩增。
