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

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 toler ance. Mice were treated continuously from birth with rabbit antimouse IgM s erum for 5 weeks. Immunohistological studies revealed that anti-IgM treatme nt 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% chic ken egg white to drink for 5 days. Anti-IgM treatment was stopped 2 days af ter the last feed. Ten weeks later, the mice were immunized with 100 mu g o valbumin emulsified with complete Frund's adjuvant. Their T helper 1 (Th1) cell-regulated systemic delayed-type hypersensitivity, IgG2a antibody respo nses and spleen cell production of interferon-r and interleukin-2 were supp ressed by prior ovalbumin or egg white feeding during anti-IgM treatment. A ctive suppression of Th1 immune responses was also demonstrated following a doptive transfer of egg white-fed donor spleen cells collected during anti- IgM treatment to naive recipients. Although enormous small resting B cells are aggregated in the mantle zones of follicles of intestinal Peyer's patch es, they are not the antigen-presenting cells seen in the induction of oral tolerance.