Adaptive immune components are thought to exert non-overlapping roles in antimicrobial host defence, with antibodies targeting pathogens in the extracellular environment and T cells eliminating infection inside cells^1,2. Reliance on antibodies for vertically transferred immunity from mothers to babies may explain neonatal susceptibility to intracellular infections^3,4. Here we show that pregnancy-induced post-translational antibody modification enables protection against the prototypical intracellular pathogen Listeria monocytogenes. Infection susceptibility was reversed in neonatal mice born to preconceptually primed mothers possessing L. monocytogenes-specific IgG or after passive transfer of antibodies from primed pregnant, but not virgin, mice. Although maternal B cells were essential for producing IgGs that mediate vertically transferred protection, they were dispensable for antibody acquisition of protective function, which instead required sialic acid acetyl esterase⁵ to deacetylate terminal sialic acid residues on IgG variable-region N-linked glycans. Deacetylated L. monocytogenes-specific IgG protected neonates through the sialic acid receptor CD22^6,7, which suppressed IL-10 production by B cells leading to antibody-mediated protection. Consideration of the maternal–fetal dyad as a joined immunological unit reveals protective roles for antibodies against intracellular infection and fine-tuned adaptations to enhance host defence during pregnancy and early life.

适应性免疫成分被认为在抗菌宿主防御中发挥非重叠作用，抗体针对细胞外环境中的病原体，T 细胞消除细胞内的感染^1,2。依赖抗体将免疫力从母亲垂直转移到婴儿可能解释了新生儿对细胞内感染的易感性^3,4。在这里，我们表明，妊娠诱导的翻译后抗体修饰能够针对典型的细胞内病原体单核细胞增生李斯特氏菌提供保护。具有单核细胞增生李斯特氏菌特异性 IgG 的孕前免疫母体所生的新生小鼠，或者从免疫过的怀孕小鼠（而非处女小鼠）被动转移抗体后，感染易感性发生逆转。尽管母体 B 细胞对于产生介导垂直转移保护的 IgG 至关重要，但它们对于抗体获得保护功能来说是可有可无的，而保护功能需要唾液酸乙酰酯酶 5 来对 IgG 可变区 N 连接聚糖上的末端唾液酸残基进行^脱乙酰化。去乙酰化单核细胞增多性李斯特菌特异性 IgG 通过唾液酸受体 CD22 ^6,7保护新生儿，抑制 B 细胞产生 IL-10，从而产生抗体介导的保护。将母胎二元体视为一个联合的免疫单位，揭示了抗体对细胞内感染的保护作用，以及微调适应以增强妊娠和早期生命期间宿主防御的作用。