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Center for Neurologic Diseases, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115
Peripheral immune tolerance following i.v. administration of Ag has
been shown to occur in the absence of B cells. Because different
mechanisms have been identified for i.v. vs low dose oral tolerance and
B cells are a predominant component of the gut-associated lymphoid
tissue (GALT) they may play a role in tolerance induction following
oral Ag. To examine the role of B cells in oral tolerance we fed low
doses of OVA or myelin oligodendrocyte glycoprotein to B cell-deficient
(µMT) and wild-type C57BL/6 mice. Results showed that the GALT of
naive wild-type and µMT mice was characterized by major differences
in the cytokine microenvironment. Feeding low doses of 0.5 mg OVA or
250 µg myelin oligodendrocyte glycoprotein resulted in up-regulation
of IL-4, IL-10, and TGF-
in the GALT of wild-type but not µMT
mice. Upon stimulation of popliteal node cells, in vitro induction of
regulatory cytokines TGF- and IL-10 was observed in wild-type but
not µMT mice. Greater protection against experimental autoimmune
encephalomyelitis was found in wild-type mice. Oral tolerance in µMT
and wild-type mice was found to proceed by different mechanisms. Anergy
was observed from 0.5 mg to 250 ng in µMT mice but not in wild-type
mice. Increased Ag was detected in the lymph of µMT mice. No
cytokine-mediated suppression was found following lower doses from 100
ng to 500 pg in either group. These results demonstrate the importance
of the B cell for the induction of cytokine-mediated suppression
associated with low doses of Ag.
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