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The Role of Chemokines in Oral Tolerance.
Author(s) -
KARPUS WILLIAM J.,
LUKACS NICHOLAS W.
Publication year - 1996
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1996.tb21122.x
Subject(s) - immunology , ccl3 , antigen , myelin basic protein , chemokine , cytokine , experimental autoimmune encephalomyelitis , immune tolerance , ccl22 , immune system , proteolipid protein 1 , biology , ccl2 , cxcl10 , myelin , endocrinology , central nervous system
Peripheral antigen-specific tolerance can be induced by feeding protein antigens. The mechanism has been described as either clonal anergy/deletion or induction of antigen-specific regulatory cells that produce transforming growth factor (TGF)-beta, depending on the dose of antigen fed. Experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, can be prevented by feeding myelin basic protein (MBP) or proteolipid protein (PLP). We decided to address the role of chemokines in the induction of oral tolerance. We have used a model antigen system of feeding a high dose of human gamma globulin (HGG) to mice that have been subsequently immunized with HGG emulsified in CFA. The result was decreased recall proliferative, delayed-type hypersensitivity (DTH) and Th1 cytokine responses. By contrast, Th2 cytokine responses were enhanced. Interestingly, macrophage inflammatory protein (MIP)-1alpha production was decreased, whereas monocyte chemotactic protein (MCP)-1 production was enhanced. Induction of oral tolerance was prevented by the administration of anti-MCP-1 to mice fed HGG. These results show that chemokines play an important role in the induction of oral tolerance.