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.

Vaccine-induced protection against Helicobacter pylori in mice lacking both antibodies and interleukin-4.

To test the hypothesis that a Th2 response to Helicobacter pylori is necessary for protection and to address the possibility that humoral and Th2 cellular responses may compensate for each other, we generated mice deficient in both interleukin-4 (IL-4) and antibodies. The immunized double-knockout mice were protected from H. pylori challenge, as were the parental strains and wild-type C57BL/6 mice.

T cell cytokines determine the severity of experimental IgA nephropathy by regulating IgA glycosylation.

Hyperfunction of Th2 cells and aberrant glycosylation of IgA have been proposed independently as factors in the pathogenesis of IgA nephropathy (IgAN), the most common form of glomerulonephritis. To investigate the relationship between Th2 cytokines and IgA glycosylation in the genesis of IgAN, we induced IgAN in C3HeB and BALB/c mice by oral immunization and intranasal challenge with Sendai virus. Although both strains of mice developed microhaematuria and glomerular IgA immune deposits to similar degrees, only BALB/c mice developed significant renal insufficiency.

Antibody-independent protective mucosal immunity to gastric helicobacter infection in mice.

Helicobacter pylori infection of the gastric mucosa can result in gastritis and peptic ulcer disease. Although vaccination can induce protective immunity in animal models of Helicobacter infection, the mechanism(s) of protective immunity has not been fully elucidated. This study was designed to determine whether humoral immune responses are required for protective Helicobacter immunity.

Oral immunization against respiratory viruses in mice.

The results presented here extend our previous observations regarding oral immunization against respiratory viruses in three areas. First, from an experiment comparing Sendai virus with influenza virus it appears that the nature of the antigen as well as host-parasite interactions may play an important role in efficiency of oral immunization. Second, oral immunization with an inactivated virus can apparently induce a cell-mediated immune response.