TY - JOUR
T1 - Nonmyelin-specific T cells accelerate development of central nervous system APC and increase susceptibility to experimental autoimmune encephalomyelitis
AU - Jones, Richard E.
AU - Kay, Thomas
AU - Keller, Thomas
AU - Bourdette, Dennis
PY - 2003/1/15
Y1 - 2003/1/15
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0037438487&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037438487&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.170.2.831
DO - 10.4049/jimmunol.170.2.831
M3 - Article
C2 - 12517947
AN - SCOPUS:0037438487
SN - 0022-1767
VL - 170
SP - 831
EP - 837
JO - Journal of Immunology
JF - Journal of Immunology
IS - 2
ER -