B-cell depletion fails to abrogate the induction of oral tolerance of specific Th1 immune responses in mice.

Abstract

Antigen presentation by resting B cells has been shown to induce peripheral tolerance to intravenous (i.v.) administered soluble protein antigens. We further examined the role of resting B cells in the induction of oral tolerance. Mice were treated continuously from birth with rabbit antimouse IgM serum for 5 weeks. Immunohistological studies revealed that anti-IgM treatment depleted B cell-aggregated follicles in intestinal Peyer's patches. At 4-weeks-old, B cell-depleted mice were fed 25 mg ovalbumin or given 10% chicken egg white to drink for 5 days. Anti-IgM treatment was stopped 2 days after the last feed. Ten weeks later, the mice were immunized with 100 microg ovalbumin emulsified with complete Frund's adjuvant. Their T helper 1 (Th1) cell-regulated systemic delayed-type hypersensitivity, IgG2a antibody responses and spleen cell production of interferon-r and interleukin-2 were suppressed by prior ovalbumin or egg white feeding during anti-IgM treatment. Active suppression of Th1 immune responses was also demonstrated following adoptive transfer of egg white-fed donor spleen cells collected during anti-IgM treatment to naïve recipients. Although enormous small resting B cells are aggregated in the mantle zones of follicles of intestinal Peyer's patches, they are not the antigen-presenting cells seen in the induction of oral tolerance.