Oral tolerance: immune mechanisms and treatment of autoimmune diseases
Reference (143)
Immunol. Today
(1987)- et al.
Cell. Immunol.
(1994) - et al.
Cell. Immunol.
(1990) - et al.
Immunol. Today
(1996) - et al.
Immunol. Lett.
(1995) Immunol. Today
(1992)- et al.
Cell. Immunol.
(1990) - et al.
J. Neuroimmunol.
(1995) - et al.
Cell. Immunol.
(1996) - et al.
Cell. Immunol.
(1988)
J. Infect. Dis.
(1911)
J. Immunol.
(1994)
J. Clin. Invest.
(1993)
J. Exp. Med.
(1993)
Annu. Rev. Immunol.
(1994)
Science
(1993)
Science
(1993)
Arthritis Rheum.
(1996)
Arthritis Rheum.
(1996)
Ann. New York Acad. Sci.
(1996)
Ann. New York Acad. Sci.
(1996)
J. Immunol.
(1991)
J. Immunol.
(1993)
Nature
(1995)
Cun. Top. Microbiol. Immunol.
(1989)
Scand. J. Immunol.
(1986)
Immunology
(1986)
Ann. New York Acad. Sci.
(1996)
J. Immunol.
(1996)
Science
(1994)
J. Immunol.
(1996)
J. Exp. Med.
(1990)
J. Immunol.
(1990)
J. Immunol.
(1992)
Nature
(1992)
J. Immunol.
(1991)
J. Exp. Med.
(1992)
J. Exp. Med.
(1996)
J. exp. Med.
(1996)
FASEB J.
(1996)
J. Clin. Invest.
(1996)
J. Immunol.
(1989)
J. Immunol.
(1990)
J. Immunol.
(1995)
Int. Immunol.
(1995)
J. Immunol.
(1996)
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