2004 年 3 巻 2 号 p. 99-104
The present study assesses the roles of the postnatal 55-kDa tumor necrosis factor (TNF) receptor (TNFR55)- or lymphotoxin-β receptor (LTβR)-mediated signals in the spleens of mice in terms of subsequent regulation of antigen-specific serum antibody responses after oral immunization. Inhibition of TNFR55-dependent signaling revealed significant reduction of germinal center (GC) formation in the spleen. Furthermore, when LTβR-dependent signaling was blocked, segregation of T and B cell areas was disrupted and the formation of GC and follicular dendritic cell (FDC) clusters was significantly reduced. TNFR55-Ig- or LTβR-Ig-treated mice with altered splenic microarchitecture continued to produce antigen-specific serum IgG and IgA antibody responses after oral immunization. However, the levels were significantly lower than those of control mice. These findings demonstrated that the splenic microarchitecture must be properly maintained for the induction of serum antibody responses after oral immunization.
