Pregnancy enables antibody protection against intracellular infection

John J. Erickson, Stephanie Archer-Hartmann, Alexander E. Yarawsky, Jeanette L. C. Miller, Stephanie Seveau, Tzu-Yu Shao, Ashley L. Severance, Hilary Miller-Handley, Yuehong Wu, Giang Pham, Brian R. Wasik, Colin R. Parrish, Yueh-Chiang Hu, Joseph T. Y. Lau, Parastoo Azadi, Andrew B. Herr and Sing Sing Way ()
Additional contact information
John J. Erickson: University of Cincinnati School of Medicine
Stephanie Archer-Hartmann: University of Georgia
Alexander E. Yarawsky: University of Cincinnati School of Medicine
Jeanette L. C. Miller: University of Cincinnati School of Medicine
Stephanie Seveau: Ohio State University
Tzu-Yu Shao: University of Cincinnati School of Medicine
Ashley L. Severance: University of Cincinnati School of Medicine
Hilary Miller-Handley: University of Cincinnati School of Medicine
Yuehong Wu: University of Cincinnati School of Medicine
Giang Pham: University of Cincinnati School of Medicine
Brian R. Wasik: Cornell University
Colin R. Parrish: Cornell University
Yueh-Chiang Hu: University of Cincinnati School of Medicine
Joseph T. Y. Lau: Roswell Park Comprehensive Cancer Center
Parastoo Azadi: University of Georgia
Andrew B. Herr: University of Cincinnati School of Medicine
Sing Sing Way: University of Cincinnati School of Medicine

Nature, 2022, vol. 606, issue 7915, 769-775

Abstract: Abstract 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 cells1,2. Reliance on antibodies for vertically transferred immunity from mothers to babies may explain neonatal susceptibility to intracellular infections3,4. 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 CD226,7, 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.

Date: 2022
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DOI: 10.1038/s41586-022-04816-9

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