Chakroun, A. | Search bioRxiv

bioRxiv2026

Serotype specific anti-capsular polysaccharide IgG associated with colonizing and invasive group B streptococcus in pregnant woman-newborn dyads

Maternal IgG against group B streptococcus (GBS) capsular polysaccharide (CPS), is the principal placental mediator of neonatal protection, yet naturally acquired anti-CPS immunity has not been characterized in North African populations. To address this gap, we conducted a prospective study in a Moroccan mother-newborn cohort to quantify the serotype-specific anti-CPS IgG levels in relation to colonizing versus invasive GBS serotypes. Additionally, we assessed the transplacental transfer of anti-CPS IgG and identified potential correlates of invasive disease. We examined serotype-specific anti-CPS IgG (serotypes Ia-V) in the plasma from maternal and cord blood of 103 GBS-colonized pregnant women, 35 uncolonized controls and their paired newborns (90 paired colonized dyads, including five newborns with invasive GBS disease) using a standardized six-plex immunoassay. Transfer ratios were compared with 1.0 and cord concentrations with published serotype- and onset-specific risk-reduction thresholds. Maternal anti-CPS IgG concentrations varied by serotype, with the highest median for serotype II(1.36g/mL) and the lowest for serotype Ib(0.003g/mL). They were higher in GBS-colonized than uncolonized mothers for serotypes Ia, Ib and II. Maternal and cord blood IgG concentrations were correlated across serotypes, but placental transfer was incomplete, with median ratios of 0.50-0.80. Among 77 newborns, 13.0%(n=10) reached early-onset and 44.2%(n=34) achieved late-onset disease risk-reduction thresholds. The serotype IV was the most identified among neonatal infection disease cases, and this was associated with sub-protective anti-serotype IV antibody. This suggests that while naturally acquired anti-serotype II antibodies were predominant, the low level of anti-serotype IV antibodies could contribute to neonatal infection diseases in mother-newborn pairs.

immunology↗

bioRxiv2020

The minor and major spliceosome interact to regulate alternative splicing around minor introns

Mutations in minor spliceosome components are linked to diseases such as Roifman syndrome, Lowry-Wood syndrome, and early-onset cerebellar ataxia (EOCA). Here we report that besides increased minor intron retention, Roifman syndrome and EOCA can also be characterized by elevated alternative splicing (AS) around minor introns. Consistent with the idea that the assembly/activity of the minor spliceosome informs AS in minor intron-containing genes (MIGs), inhibition of all minor spliceosome snRNAs led to upregulated AS. Notably, alternatively spliced MIG isoforms were bound to polysomes in the U11-null dorsal telencephalon, which suggested that aberrant MIG protein expression could contribute to disease pathogenesis. In agreement, expression of an aberrant isoform of the MIG Dctn3 by in utero electroporation, affected radial glial cell divisions. Finally, we show that AS around minor introns is executed by the major spliceosome and is regulated by U11-59K of the minor spliceosome, which forms exon-bridging interactions with proteins of the major spliceosome. Overall, we extend the exon-definition model to MIGs and postulate that disruptions of exon-bridging interactions might contribute to disease severity and pathogenesis.

molecular biology↗