Gustafsson E, Mattsson A, Holmdahl R, Mattsson R
Department of Animal Development and Genetics, Uppsala University, Sweden.
Biol Reprod. 1994 Dec;51(6):1173-80. doi: 10.1095/biolreprod51.6.1173.
Mice lacking functional B cells because of a genetic deletion of the mu chain (IgM) gene were used to investigate the role of perinatal and postnatal transfer of maternal IgG in neonatal growth. Our results confirmed that immunoglobulin (Ig)-deficient mice successfully complete pregnancy and deliver healthy offspring. However, neonates nursed by Ig-deficient mothers showed growth retardation (runting) and high mortality during their first 10 days of life. This fatal course was seen whether or not the neonates were Ig-deficient. Cross-switching litters from phenotypically normal mothers to Ig-deficient mothers immediately after birth showed that perinatal Ig transfer normalized neonatal development for 10 days, but was not sufficient to sustain survival during the later part of the neonatal period. On the other hand, all Ig-deficient litters nursed by normal foster mothers showed normal development and 0% neonatal mortality. Administration of mouse IgG to an Ig-deficient mother or a neonate during the first critical week prevented runting. We assume that the growth- and health-promoting effects of IgG during early neonatal life are attributable mainly to the transfer of passive immunity to environmental pathogens. However, the finding that monoclonal IgG antibodies also enhanced neonatal growth and survival suggests that IgG-dependent growth-promoting mechanisms could be involved as well.
由于μ链（IgM）基因的基因缺失而缺乏功能性B细胞的小鼠被用于研究围产期和产后母体IgG转移在新生儿生长中的作用。我们的结果证实，免疫球蛋白（Ig）缺陷小鼠成功完成妊娠并产下健康后代。然而，由Ig缺陷母亲哺乳的新生儿在出生后的头10天内出现生长迟缓（发育不良）和高死亡率。无论新生儿是否Ig缺陷，都会出现这种致命的情况。出生后立即将表型正常母亲的同窝仔鼠与Ig缺陷母亲的同窝仔鼠进行交叉交换，结果表明围产期Ig转移使新生儿发育在10天内恢复正常，但不足以维持新生儿后期的存活。另一方面，由正常代孕母亲哺乳的所有Ig缺陷同窝仔鼠均表现出正常发育，新生儿死亡率为0%。在第一个关键周内给Ig缺陷母亲或新生儿注射小鼠IgG可防止发育不良。我们认为，新生儿早期生活中IgG对生长和健康的促进作用主要归因于对环境病原体的被动免疫转移。然而，单克隆IgG抗体也能促进新生儿生长和存活这一发现表明，IgG依赖性生长促进机制也可能起作用。
