Myelin basic protein-specific T lymphocytes induce chronic relapsing experimental autoimmune encephalomyelitis in lymphocyte-deficient (SCID) mice

Citation
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
Citations number
37
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROIMMUNOLOGY
ISSN journal
01655728 → ACNP
Volume
93
Issue
1-2
Year of publication
1999
Pages
92 - 101
Database
ISI
SICI code
0165-5728(19990101)93:1-2<92:MBPTLI>2.0.ZU;2-A
Abstract
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.