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Chronic neurologic dysfunction and demyelination induced in Lewis rats by repeated injections of encephalitogenic T-lymphocyte lines.
J Neurosci Res. 1986; 16(4):643-56.JN

Abstract

Experimental autoimmune encephalomyelitis (EAE) in the Lewis rat is characteristically a monophasic paralytic disorder. Recovered rats are thereafter immune to EAE induced by injection of guinea pig basic protein (GP-BP) in complete Freund's adjuvant (CFA), but they are still susceptible to EAE induced by an encephalitogenic T-lymphocyte line (BP-1). Induction of active EAE or injection of a sublethal dose of activated BP-1 cells resulted in a monophasic episode of EAE, followed by recovery of normal neurologic function. Repeated challenges with activated BP-1 cells, however, induced unremitting neurologic signs marked by loss of tail tonicity and incontinence, which persisted for more than 6 months. Histologically, the spinal cord of affected rats revealed attenuation of MBP staining (demyelination) and moderate-to-extensive gliosis associated with increased size of intervening spaces. Inflammatory cell lesions, however, were notably absent. Biophysical analysis of isolated spinal cord myelin from affected rats demonstrated a distorted distribution in subfraction densities and the appearance of extra-myelin proteins in the light myelin subfraction. Immunologically, chronically affected animals were unresponsive to the encephalitogenic determinant on GP-BP, although other BP determinants elicited strong delayed type hypersensitivity (DTH) reactions in rats immunized initially with GP-BP in CFA. These data show that ongoing neurologic dysfunction can be induced in the Lewis rat by a GP-BP specific T-lymphocyte line; they suggest that unremitting clinical signs can persist in the absence both of inflammatory lesions in the CNS and of pronounced immunologic responsiveness to the encephalitogenic determinant of GP-BP.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

2432277

Citation

Vandenbark, A A., et al. "Chronic Neurologic Dysfunction and Demyelination Induced in Lewis Rats By Repeated Injections of Encephalitogenic T-lymphocyte Lines." Journal of Neuroscience Research, vol. 16, no. 4, 1986, pp. 643-56.
Vandenbark AA, Nilaver G, Konat G, et al. Chronic neurologic dysfunction and demyelination induced in Lewis rats by repeated injections of encephalitogenic T-lymphocyte lines. J Neurosci Res. 1986;16(4):643-56.
Vandenbark, A. A., Nilaver, G., Konat, G., Teal, P., & Offner, H. (1986). Chronic neurologic dysfunction and demyelination induced in Lewis rats by repeated injections of encephalitogenic T-lymphocyte lines. Journal of Neuroscience Research, 16(4), 643-56.
Vandenbark AA, et al. Chronic Neurologic Dysfunction and Demyelination Induced in Lewis Rats By Repeated Injections of Encephalitogenic T-lymphocyte Lines. J Neurosci Res. 1986;16(4):643-56. PubMed PMID: 2432277.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chronic neurologic dysfunction and demyelination induced in Lewis rats by repeated injections of encephalitogenic T-lymphocyte lines. AU - Vandenbark,A A, AU - Nilaver,G, AU - Konat,G, AU - Teal,P, AU - Offner,H, PY - 1986/1/1/pubmed PY - 1986/1/1/medline PY - 1986/1/1/entrez SP - 643 EP - 56 JF - Journal of neuroscience research JO - J Neurosci Res VL - 16 IS - 4 N2 - Experimental autoimmune encephalomyelitis (EAE) in the Lewis rat is characteristically a monophasic paralytic disorder. Recovered rats are thereafter immune to EAE induced by injection of guinea pig basic protein (GP-BP) in complete Freund's adjuvant (CFA), but they are still susceptible to EAE induced by an encephalitogenic T-lymphocyte line (BP-1). Induction of active EAE or injection of a sublethal dose of activated BP-1 cells resulted in a monophasic episode of EAE, followed by recovery of normal neurologic function. Repeated challenges with activated BP-1 cells, however, induced unremitting neurologic signs marked by loss of tail tonicity and incontinence, which persisted for more than 6 months. Histologically, the spinal cord of affected rats revealed attenuation of MBP staining (demyelination) and moderate-to-extensive gliosis associated with increased size of intervening spaces. Inflammatory cell lesions, however, were notably absent. Biophysical analysis of isolated spinal cord myelin from affected rats demonstrated a distorted distribution in subfraction densities and the appearance of extra-myelin proteins in the light myelin subfraction. Immunologically, chronically affected animals were unresponsive to the encephalitogenic determinant on GP-BP, although other BP determinants elicited strong delayed type hypersensitivity (DTH) reactions in rats immunized initially with GP-BP in CFA. These data show that ongoing neurologic dysfunction can be induced in the Lewis rat by a GP-BP specific T-lymphocyte line; they suggest that unremitting clinical signs can persist in the absence both of inflammatory lesions in the CNS and of pronounced immunologic responsiveness to the encephalitogenic determinant of GP-BP. SN - 0360-4012 UR - https://www.unboundmedicine.com/medline/citation/2432277/Chronic_neurologic_dysfunction_and_demyelination_induced_in_Lewis_rats_by_repeated_injections_of_encephalitogenic_T_lymphocyte_lines_ L2 - https://doi.org/10.1002/jnr.490160406 DB - PRIME DP - Unbound Medicine ER -