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Departments of
*
Microbiology-Immunology and
Pathology and the Interdepartmental Immunobiology Center, Northwestern University Medical School and the Northwestern University Institute for Neuroscience, Chicago, IL 60611;
Ben May Institute for Cancer Research and the Committee for Immunology, University of Chicago, Chicago, IL 60637; and
§
Immunology Research Division, Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115
The B7/CD28 pathway provides critical costimulatory signals
required for complete T cell activation and has served as a potential
target for immunotherapeutic strategies designed to regulate autoimmune
diseases. This study was designed to examine the roles of CD28 and its
individual ligands, B7-1 and B7-2, in experimental autoimmune
encephalomyelitis (EAE), a Th1-mediated inflammatory disease of the
CNS. EAE induction in CD28- or B7-deficient nonobese diabetic (NOD)
mice was compared with the effects of B7/CD28 blockade using Abs in
wild-type NOD mice. Disease severity was significantly reduced in
CD28-deficient as well as anti-B7-1/B7-2-treated NOD mice. B7-2
appeared to play the more dominant role as there was a moderate
decrease in disease incidence and severity in B7-2-deficient animals.
EAE resistance was not due to the lack of effective priming of the
myelin peptide-specific T cells in vivo. T cells isolated from
CD28-deficient animals produced equivalent amounts of IFN-
and
TNF-
in response to the immunogen, proteolipid protein 56–70. In
fact, IFN- and TNF- production by Ag-specific T cells was
enhanced in both the B7-1 and B7-2-deficient NOD mice. In contrast,
peptide-specific delayed-type hypersensitivity responses in these
animals were significantly decreased, suggesting a critical role for
CD28 costimulation in in vivo trafficking and systemic immunity.
Collectively, these results support a critical role for CD28
costimulation in EAE induction.
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