Role of maternal antibody in the induction of virus specific and bystander IgA responses in Peyer's patches of suckling mice

Reciprocal crossings of C.B17 scid/scid and congenic BALB/c ( +/+ ) mice generate genetically identical, immunocompetent F1 scid/+ mice that develop in either the absence or influence of passively transferred maternal immunity. By exchanging F1 scid/+ litters at birth among scid/scid, non-immune or...

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Veröffentlicht in:International immunology 1995-06, Vol.7 (6), p.911-918
Hauptverfasser: Kramer, David R., Cebra, John J.
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Sprache:eng
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Zusammenfassung:Reciprocal crossings of C.B17 scid/scid and congenic BALB/c ( +/+ ) mice generate genetically identical, immunocompetent F1 scid/+ mice that develop in either the absence or influence of passively transferred maternal immunity. By exchanging F1 scid/+ litters at birth among scid/scid, non-immune or reovirus immune BALB/c mothers we examined the relative ability of placental or colostral/milk transfer of virus specific maternal antibodies to interfere with reovirus immunization of the neonatal gut associated lymphold tissues (GALT). Our data demonstrate that the Peyer's patches (PP) in 10-day-old mice are competent to support thymus dependent responses to acute reovirus stimulation that include the rapid (within 3 days) development of specific IgA plasma cells and the subsequent initiation of PP germinal center reactions. These neonatal mucosal immune responses occur independently of coincident specific maternal immune responses as evidenced by the identity of the reovirus specific responses engendered in F1 scid/+ pups of scid/scid versus +/+ mothers. However, transfer of pre-existing reovirus specific maternal antibody in milk via nursing on a reovirus immune (foster) mother completely abrogated reovirus specific neonatal IgA responses; while placental transfer of specific maternal antibody alone did not interfere with the immunization of the neonatal GALT with enteric reovirus. Reovirus challenge of 10-day-old mice was associated with a substantial bystander IgA response. Possible mechanisms responsible for the induction of the observed bystander IgA responses are discussed.
ISSN:0953-8178
1460-2377
DOI:10.1093/intimm/7.6.911