The Neonate Fc Receptor (FcRn) For IgG Is Important For The Development of Rotavirus-Specific IgG Responses And Clearance of Rotavirus From The Intestines Of Mice (53.5)

Abstract Rotavirus infection and virus-like particle vaccines induce intestinal rotavirus-specific IgG in mice that appears to play a role in protection. The mechanism by which rotavirus-specific IgG reaches the intestinal lumen is unknown. The neonatal Fc receptor for IgG (FcRn) is the only known t...

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Bibliographic Details
Published inThe Journal of immunology (1950) Vol. 178; no. 1_Supplement; p. S104
Main Authors Marcelin, Glendie, Conner, Margaret E
Format Journal Article
LanguageEnglish
Published 01.04.2007
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Summary:Abstract Rotavirus infection and virus-like particle vaccines induce intestinal rotavirus-specific IgG in mice that appears to play a role in protection. The mechanism by which rotavirus-specific IgG reaches the intestinal lumen is unknown. The neonatal Fc receptor for IgG (FcRn) is the only known transporter of IgG in the intestines in neonatal and adult mice. Additionally, FcRn is implicated in antigen presentation in the intestines of adult mice. We tested whether FcRn is important in protecting the intestine against rotavirus infection and in transport of rotavirus-specific IgG into the intestinal lumen. Naïve FcRn deficient (FcRn−/−) and wild type BALB/c controls were orally inoculated with 103ID50 ECWT rotavirus. Fecal samples were collected 0–12 days post inoculation (dpi) and tested for rotavirus antigen and rotavirus-specific IgG by ELISA. Virus clearance from the intestine was significantly delayed by 3 days in FcRn−/− compared to BALB/c mice. Rotavirus-specific intestinal IgG titers were also significantly lower in FcRn−/− versus BALB/c mice. These data indicate that FcRn plays a role in clearance of a primary rotavirus infection from the intestine and intestinal transport of rotavirus-specific IgG. Studies are underway to elucidate the mechanism(s) by which FcRn contributes to clearance of intestinal rotavirus infection. VA Merit Review Grant, NIH RO1 AI24998
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.178.Supp.53.5