J Immunol 2003 Jan 15;170(2):831-7
Jones RE, Kay T, Keller T, Bourdette D.
Veterans Affairs Medical Center, Departments of Neurology and Microbiology and Molecular Immunology, Oregon Health & Science University, and Oregon Cancer Institute, Portland, OR 97239.
Previously we demonstrated that both myelin-specific and nonmyelin-specific rat T cells were capable of accelerating the development of transplanted rat BM-derived APC in the CNS of SCID C.B-17/scid (SCID) mice.
This suggested that nonmyelin-specific T cells might be capable of increasing susceptibility to EAE by increasing the number and function of APC in the CNS before disease induction.
To assess this possibility, we evaluated disease incidence, day of onset, duration, mean peak severity, cumulative disease index, and histopathology in the presence or absence of nonmyelin-specific T cells.
The results demonstrate an association between T cell responses to nonmyelin Ags, accelerated development of BM-derived CNS APC before disease induction, and heightened susceptibility to CNS inflammation mediated by myelin-specific T cells.
This suggests that T cell responses to nonmyelin Ags can potentiate CNS inflammation by elevating the functional presence of CNS APC.