4.8 Article

Compromised SARS-CoV-2-specific placental antibody transfer

期刊

CELL
卷 184, 期 3, 页码 628-+

出版社

CELL PRESS
DOI: 10.1016/j.cell.2020.12.027

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资金

  1. Ragon Institute of MGH, MIT and Harvard
  2. NIH [3R37AI080289-11S1, R01AI146785, U19AI42790-01, U19AI135995-02, 1U01CA260476 -01, CIVIC5N93019C00052]
  3. Gates Foundation Global Health Vaccine Accelerator Platform [OPP1146996, INV001650]
  4. Musk Foundation
  5. Terry and Susan Ragon Research Scholars award
  6. SAMANA Kay MGH Research Scholars award

向作者/读者索取更多资源

SARS-CoV-2 infection causes more severe disease in pregnant women compared to age-matched non-pregnant women. Transfer of SARS-CoV-2-specific antibodies across the placenta is significantly reduced compared to other infectious diseases like influenza and pertussis, but can be partially rescued by infection-induced increases in IgG and increased FCGR3A placental expression. These findings provide insights for maternal vaccine design to boost immunity in neonates.
SARS-CoV-2 infection causes more severe disease in pregnant women compared to age-matched non-pregnant women. Whether maternal infection causes changes in the transfer of immunity to infants remains unclear. Maternal infections have previously been associated with compromised placental antibody transfer, but the mechanismunderlying this compromised transfer is not established. Here, we used systems serology to characterize the Fc profile of influenza-, pertussis-, and SARS-CoV-2-specific antibodies transferred across the placenta. Influenza- and pertussis-specific antibodies were actively transferred. However, SARS-CoV-2-specific antibody transfer was significantly reduced compared to influenza- and pertussis-specific antibodies, and cord titers and functional activity were lower than in maternal plasma. This effect was only observed in third-trimester infection. SARS-CoV-2-specific transfer was linked to altered SARS-CoV2-anti-body glycosylation profiles and was partially rescued by infection-induced increases in IgG and increased FCGR3A placental expression. These results point to unexpected compensatory mechanisms to boost immunity in neonates, providing insights for maternal vaccine design.

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