Pregnancy enables antibody protection against intracellular infection.

Autor: Erickson JJ; Department of Pediatrics, Division of Infectious Diseases, Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA.; Department of Pediatrics, Division of Neonatology, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA., Archer-Hartmann S; Complex Carbohydrate Research Center, University of Georgia, Athens, GA, USA., Yarawsky AE; Department of Pediatrics, Division of Immunobiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA., Miller JLC; Department of Pediatrics, Division of Immunobiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA., Seveau S; Department of Microbial Infection and Immunity, Ohio State University, Columbus, OH, USA., Shao TY; Department of Pediatrics, Division of Infectious Diseases, Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA., Severance AL; Department of Pediatrics, Division of Infectious Diseases, Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA., Miller-Handley H; Department of Pediatrics, Division of Infectious Diseases, Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA.; Department of Internal Medicine, Division of Infectious Diseases, University of Cincinnati School of Medicine, Cincinnati, OH, USA., Wu Y; Department of Pediatrics, Division of Infectious Diseases, Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA., Pham G; Department of Pediatrics, Division of Infectious Diseases, Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA., Wasik BR; Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA., Parrish CR; Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA., Hu YC; Department of Pediatrics, Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA., Lau JTY; Department of Molecular and Cell Biology, Roswell Park Comprehensive Cancer Center, Buffalo, NY, USA., Azadi P; Complex Carbohydrate Research Center, University of Georgia, Athens, GA, USA., Herr AB; Department of Pediatrics, Division of Immunobiology, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA., Way SS; Department of Pediatrics, Division of Infectious Diseases, Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, University of Cincinnati School of Medicine, Cincinnati, OH, USA. singsing.way@cchmc.org.
Jazyk: angličtina
Zdroj: Nature [Nature] 2022 Jun; Vol. 606 (7915), pp. 769-775. Date of Electronic Publication: 2022 Jun 08.
DOI: 10.1038/s41586-022-04816-9
Abstrakt: 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 esterase 5 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.
(© 2022. The Author(s), under exclusive licence to Springer Nature Limited.)
Databáze: MEDLINE
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