Re. Jones et al., Myelin basic protein-specific T lymphocytes induce chronic relapsing experimental autoimmune encephalomyelitis in lymphocyte-deficient (SCID) mice, J NEUROIMM, 93(1-2), 1999, pp. 92-101
Myelin basic protein (BP)-specific T lymphocyte cell lines were selected fr
om the lymph nodes (LN) of BP-immunized, H-2(d), CXJ-1 mice prior to the on
set of clinical disease. These CD4 + T cells induced severe acute experimen
tal autoimmune encephalomyelitis (EAE) in MHC-compatible (N-2(d)), lymphocy
te-deficient (SCID) mice (C.B-17scid/scid). The incidence of disease was mu
ch higher in immunodeficient SCID mice (71%) than in syngeneic immunocompet
ent CXJ-1 mice (5%). SCID mice with EAE had an acute progressive paralytic
disease with inflammation and myelin loss detected in the spinal cord. Eigh
ty-six percent (12/14) of mice followed for more than 2 weeks had 1 or more
relapses of EAE. These results demonstrate that clinical remission and rel
apse of EAE can be induced by the single adoptive transfer of a LN-derived
BP-specific T cell line in the absence of host-derived effector and regulat
ory lymphocytes. Furthermore, the data demonstrate that the pathogenic pote
ntial of BP-specific T cells is greater in lymphocyte-deficient SCID mice c
ompared with immunocompetent mice, suggesting that autoreactive T cells are
controlled by potent inhibitory mechanisms associated with regulatory lymp
hocytes. These results are relevant to mechanisms of disease remission and
relapse mediated by lymphocytes involved in paralytic inflammatory diseases
such as multiple sclerosis (MS). (C) 1999 Elsevier Science B.V. All rights
reserved.