The role of nasal tolerance in a model of IgA nephropathy induced in mice by Sendai virus.
Mucosal antigenic exposure is implicated in pathogenesis of IgA nephropathy. Although IgG and/or IgM codeposits may promote disease, protracted mucosal antigenic exposure reduces IgG and IgM antibody, a process termed mucosal tolerance. We immunized mice intranasally with infectious or inactivated Sendai virus for 6 or 14 weeks. Anti-virus IgG remained high in mice given infectious virus for 14 weeks, but decreased after 6 weeks in mice given inactivated virus; IgA antibody remained high in both groups. Upon viral challenge, glomerular IgG and complement deposits and the frequency of hematuria, all equal after 6 weeks of immunization, were lower in mice immunized with inactivated virus for 14 weeks but remained high in mice given infectious virus; glomerular IgA increased over time in both immunized groups. Viremia in a non-tolerized immune host can promote glomerulonephritis with IgG and complement codeposits and glomerular dysfunction. These preliminary experiments may guide future, more mechanistic, investigation.
Amore
A
A
Department of Nephrology and Dialysis, Regina Margherita Hospital, Turin, Italy.
Coppo
R
R
Nedrud
J G
JG
Sigmund
N
N
Lamm
M E
ME
Emancipator
S N
SN
D000818:Animals; D005455:Fluorescent Antibody Technique; D006417:Hematuria / Q000276:immunology; D007105:Immune Complex Diseases / Q000276:immunology; D018928:Immunity, Mucosal; D007070:Immunoglobulin A / Q000097:blood / Q000276:immunology*; D007668:Kidney / Q000276:immunology; D007674:Kidney Diseases / Q000276:immunology*; D051379:Mice; D011507:Proteinuria / Q000276:immunology; D010253:Respirovirus Infections / Q000276:immunology*; D029082:Sendai virus / Q000276:immunology*
D007070:Immunoglobulin A