myelin-basic-protein has been researched along with Leukopenia* in 2 studies
2 other study(ies) available for myelin-basic-protein and Leukopenia
| Article | Year |
|---|---|
Evidence for target tissue regulation of resistance to the induction of experimental allergic encephalomyelitis in AO rats.
A myelin basic protein (MBP)-specific T cell line derived from F1 hybrids between experimental allergic encephalomyelitis (EAE)-susceptible DA (RT1avl) strain and EAE-resistant AO (RT1u) strain was capable of inducing clinical EAE in F1 hybrids and DA, but not in AO rats. In vitro restimulation with MBP presented by AO antigen-presenting cells (APC) resulted in the generation of a MBP-specific subline restricted by RT1u MHC products which induced clinical EAE in F1 hybrids but not in the AO parental strain. Deletion of hosts' leukocytes using sublethal irradiation and cytotoxic drugs did not abrogate the resistance of AO rats, which argues against the involvement of hosts' lymphoid cells in the regulation of autoagression. Thus, mechanism(s) regulating the activity of autoagressive T cells on functional elements in the target tissue might be responsible for differences in susceptibility to EAE. Topics: Animals; Antigen-Presenting Cells; CD4-Positive T-Lymphocytes; Disease Susceptibility; Dose-Response Relationship, Immunologic; Encephalomyelitis, Autoimmune, Experimental; Epitopes; Flow Cytometry; Histocompatibility Antigens; Immunization, Passive; Leukopenia; Lymphocyte Activation; Myelin Basic Protein; Rats; Rats, Inbred Strains | 1992 |
Experimental allergic encephalomyelitis in the absence of a classical delayed-type hypersensitivity reaction. Severe paralytic disease correlates with the presence of interleukin 2 receptor-positive cells infiltrating the central nervous system.
One characteristic of experimental allergic encephalomyelitis (EAE) in all species is the presence of a considerable leukocyte infiltrate in the central nervous system (CNS). By adoptive transfer of EAE into irradiated or nonirradiated Lewis strain rats we now show that the bulk (greater than 90%) of infiltrating cells in the CNS are superfluous to the induction of disease, as lethally irradiated recipients, despite having very few infiltrating cells in the CNS, acquire severe paralytic EAE. The reduction in the level of infiltration in irradiated recipients is selective, however, as both irradiated and nonirradiated diseased animals have very similar numbers of cells expressing IL-2-R. Disease in irradiated recipient animals is associated with substantial submeningeal hemorrhage in the spinal cord and brain stem and similar hemorrhages are found in recipients rendered leukopenic with cytotoxic drugs. Clinical signs of disease and hemorrhage are preventable, however, by administration to the recipient rats of mAbs specific for the CD4 antigen. Classic delayed-type hypersensitivity (DTH) reactions are transferable with the same cells that produce EAE in both irradiated and nonirradiated recipient rats, but such transfer of DTH is observed only in nonirradiated recipient animals and not in irradiated rats. Collectively, the findings reported herein support the conclusion that the paralysis characteristic of acute EAE is mediated by the direct action of very small numbers of activated CD4+ lymphocytes that infiltrate the CNS and produce their effects by inducing vascular damage. The findings are not consistent with reports that the lesions in EAE are produced by a classic DTH reaction. Topics: Animals; Busulfan; Cells, Cultured; Central Nervous System; Cerebral Hemorrhage; Chlorambucil; Encephalomyelitis, Autoimmune, Experimental; Female; Hemorrhage; Hypersensitivity, Delayed; Immunization, Passive; Leukopenia; Male; Myelin Basic Protein; Ovalbumin; Rats; Rats, Inbred Lew; Receptors, Immunologic; Receptors, Interleukin-2; Spinal Cord Diseases; Spleen; T-Lymphocytes, Helper-Inducer; Whole-Body Irradiation | 1987 |