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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spleen cells from rats that have recovered from experimental autoimmune encephalomyelitis (EAE) suppress the production of IFN-gamma by effector T cells of EAE in an Ag-specific manner. These postrecovery suppressor cells also inhibit EAE in vivo. Fractionation of the postrecovery suppressor spleen cells on nylon wool and OX-8 coated plates yields a nylon wool-adherent CD4+ suppressor cell population that, when cocultured with effector T cells, suppresses IFN-gamma production by these effector cells. In contrast, the nylon wool-adherent, CD4+ postrecovery suppressor cell population fails to inhibit the production of IL-2 by the effector T cells. In further experiments, the effector T cell population was depleted of CD8+ cells and cocultured with the nylon wool-adherent, CD4+ postrecovery suppressor cells, and the supernatants were assayed for IFN-gamma and IL-2. IFN-gamma production was inhibited in these cultures but IL-2 production was not inhibited. Irradiated effector T cells were cocultured with CD4+ postrecovery suppressor cells, without myelin basic protein, in an effort to determine whether the mechanism of differential lymphokine suppression involved an anti-idiotypic response against effector T cells. No IL-2 was produced, indicating that there was no CD4+ suppressor cell mediated anti-idiotypic response against effector T cells. These studies suggest that the suppressor cell is a nylon wool adherent, CD4+ T cell that functions to down-regulate EAE effector T cells by differential inhibition of lymphokine production.
J Immunol 1989 Dec 01
PMID:CD4+ suppressor cells differentially affect the production of IFN-gamma by effector cells of experimental autoimmune encephalomyelitis. 257 35

The production and characterization of an anti-guinea pig B cell monoclonal antibody is described. Immunocytochemical techniques using this antibody and others recognizing a Pan T cell antigen and T cell subsets were employed to study frozen sections of spinal cord from guinea pigs with chronic relapsing experimental allergic encephalomyelitis. T and B cells were found in both perivascular lesions and the central nervous system parenchyma, with the major T cell infiltration occurring by the end of the acute phase of disease. The distribution of T cell subsets suggests a phenotypic selectivity in favour of the transport of CT6 (putative CD8)+ve cells across the blood-brain barrier.
J Neuroimmunol 1989 Dec
PMID:A quantitative immunocytochemical study of the infiltrating lymphocytes in the spinal cord of guinea pigs with chronic relapsing experimental allergic encephalomyelitis. 258 95

Mechanisms involved in the loss of blood-brain barrier function in Lewis rats with experimental autoimmune encephalomyelitis (EAE) were examined using horseradish peroxidase (HRP) as a tracer. In animals injected with HRP before fixation, tracer was observed in two intracytoplasmic compartments: multivesicular bodies (presumably secondary lysosomes) and transcytotic vesicles. Quantitative morphometry of electron micrographs of capillary endothelial cells demonstrated a 5.2-fold increase in these vesicles. This increase in vesicular transport was associated with a decrease in mitochondrial content from 13.7% of the endothelial cytoplasmic area in the normal rat to 4.2% in EAE rats at the height of clinical disease. These alterations correlated with the clinical course of EAE. In animals infused with tracer after fixation, tracer was restricted to areas of cellular inflammation. Immunogold staining of endogenous albumin demonstrated the presence of albumin in cytoplasmic vesicles and in channel-like tubular structures adjacent to endothelial cell junctions. These results indicate that there is a role for vesicles in transendothelial cell transport and edema formation in animals with EAE.
Am J Pathol 1989 Dec
PMID:Increased vesicular transport and decreased mitochondrial content in blood-brain barrier endothelial cells during experimental autoimmune encephalomyelitis. 259 75

Severe hypothermia and an ascending impairment of shivering are previously undescribed clinical signs in hyperacute experimental allergic encephalomyelitis (EAE) in the Lewis rat. These occurred in hyperacute EAE induced by inoculation with guinea pig spinal cord homogenate and heat-killed Bordetella pertussis. Hypothermia was first detected on day 6-7 post-inoculation, within 12-24 h of the onset of neurological signs, and became more severe as the disease progressed. Rectal temperatures less than or equal to 30 degrees C were common at ambient temperatures of 19-22 degrees C. Shivering was assessed by palpation and by cold tremor electromyography. Shivering was absent in the tail by day 6-7 post-inoculation. The impairment then progressed to affect the hindlimbs, thorax and occasionally the forelimbs. Shivering was absent in hindlimbs with only mild or moderate weakness. Histological studies revealed perivascular inflammation with polymorphonuclear and mononuclear cells, oedema, fibrin deposition, haemorrhage, primary demyelination and axonal degeneration in the spinal cord, dorsal root ganglia and spinal roots. The brainstem was also involved but the cerebral hemispheres, including the hypothalamus, were spared. The close relationship between the severity of hypothermia and the extent of shivering impairment indicates that reduced shivering is an important cause of hypothermia in hyperacute EAE. It is concluded that this impairment of shivering is due not to hypothalamic damage but to lesions elsewhere in the central and peripheral nervous systems.
J Neurol Sci 1989 Dec
PMID:Hypothermia due to an ascending impairment of shivering in hyperacute experimental allergic encephalomyelitis in the Lewis rat. 261 69

Two cases of disseminated vasculomyelinopathy (one of acute disseminated encephalomyelitis (ADEM), the other of acute transverse myelitis), are reported because of the persistence, 3 years and 5 months respectively, of abnormalities of magnetic resonance imaging (MRI). These abnormalities remained although in the first case the disease had been essentially asymptomatic from the onset except for one seizure, the patient remaining neurologically intact, whereas in the second case, the patient had made a complete recovery from very serious neurologic dysfunction. The first case illustrates the fact that ADEM may rarely occur without any symptoms, even in the presence of severe imaging abnormalities in both CT and MRI. Neither the persistence of a blood-brain barrier permeability alteration nor gliosis can satisfactorily explain the MRI changes, and thus the pathological significance of areas of increased signal intensity in MRI remains poorly understood and a matter of uncertainty. This report emphasizes the futility of attempting to correlate any kind of clinical observation, laboratory parameter, or effect of therapeutic regimens with changes, or lack thereof, in the MRI in multiple sclerosis and disseminated vasculomyelinopathy.
J Neurol Sci 1989 Dec
PMID:Magnetic resonance imaging in asymptomatic disseminated vasculomyelinopathy. 261 77

In Switzerland 5-35% of Ixodes ricinus ticks are infested with Borrelia burgdorferi (B.b.). There is a high risk of transmission of this infectious agent from any tick bite and 4-5% of affected subjects subsequently contract evident Lyme borreliosis. However, both tick bite and erythema chronicum migrans are unreliable diagnostic pointers as they are not usually found in the history of Lyme borreliosis patients. Similarly, an increased titer of antibodies against B.b. is not evidence of Lyme borreliosis, since this increased titer is found in some 10% of the healthy population. Finally, even a negative antibody titer does not rule out the diagnosis. The special problems of diagnosis are investigated in 7 patients with articular Lyme borreliosis and 9 patients with CNS symptoms. Articular Lyme borreliosis must be diagnosed by elimination even where there is an increased titer of antibodies against B.b., since neither the clinical picture, nor laboratory analysis of the synovial fluid, nor histologic and radiologic investigations show specific findings. There is a wide spectrum of neurologic symptoms. Diagnosis is easiest in cases with typical clinical findings (meningopolyneuritis), but in all other cases it is still by elimination. Among laboratory tests, calculation of an antibody index has proven helpful. Nevertheless, it is not always possible to differentiate Lyme borreliosis from encephalomyelitis disseminata. Antibiotic treatment has been tried in doubtful cases.
Schweiz Med Wochenschr 1989 Dec 30
PMID:[Diagnostic possibilities and limitations in Lyme borreliosis]. 269 51

Humoral antibody responses to Theiler's murine encephalomyelitis virus (TMEV) capsid proteins were examined. Rabbit antisera produced against the native BeAn strain of TMEV and against the isolated capsid proteins (VP1, VP2 and VP3) were tested for their ability to bind or neutralize virus and to inhibit the virus-induced haemagglutination of human O+ erythrocytes. Western immunoblotting analysis showed that isolated VP1, VP2 and VP3 each primed for a specific antibody response, but that native virions primed for antibodies specific for VP1 and VP2, but not VP3. Virus neutralization studies revealed that a dominant TMEV neutralizing determinant(s) lay on VP1, as did the haemagglutinating determinant. The possible location of the neutralizing epitopes are discussed on the basis of molecular modelling of the predicted amino acid sequence of TMEV from that of the closely related Mengo virus for which the three-dimensional structure is known.
J Gen Virol 1987 Dec
PMID:Characterization and specificity of humoral immune responses to Theiler's murine encephalomyelitis virus capsid proteins. 282 57

In this study, pretreatment of Lewis rats with a syngeneic encephalitogenic T cell line (S1) was found to be able to constantly induce resistance to the subsequent induction of transferred experimental autoimmune encephalomyelitis (tEAE). This treatment was capable of protecting recipient animals for at least 2-4 months. Here we show an enhanced suppressor T(anti-S1) cell activity, which can be readily detected in the lymphoid organs of animals which recovered from S1-induced tEAE, or from rats pretreated with attenuated (irradiated, fixative treated or water-lysed) S1 cells. Anti-S1 cells, which uniformly express the CD8 phenotype, were selectively stimulated to grow and expand into lines by confronting primed lymphoid cells with irradiated S1 cells in culture. The proliferative response of anti-S1 cells was independent of myelin basic protein and antigen-presenting cells, and the responses against unrelated encephalitogenic T cell lines were minimal. It was also found that none of the monoclonal antibodies tested (including CD8 and MHC class I antigen-specific antibodies) was able to block S1/anti-S1 interactions. These cells are functionally suppressive to the proliferation of S1 cells in vitro, are specifically cytolytic directed against the EAE-inducing S1 cells and are able to antagonize encephalitogenic capacity of S1 cells in vivo. In vivo elimination of the CD8+ T subset from Lewis rats, using a combined treatment of thymectomy and OX-8 antibody injection before the initial cell transfer, totally blocked the induction of resistance. Our experiments document that induction of functionally active suppressor T cells is responsible for the induced resistance observed in tEAE.
Eur J Immunol 1988 Dec
PMID:Regulatory circuits in autoimmunity: recruitment of counter-regulatory CD8+ T cells by encephalitogenic CD4+ T line cells. 290 95

Treatment with cyclosporin A, from the time of virus infection, suppressed inflammation and demyelination in the spinal cord of SJL/J or ASW(H-2s) mice persistently infected with Theiler's murine encephalomyelitis virus. Demyelination was not decreased if treatment was given after inflammation was established. The decrease was independent of serum titers of immunoglobulin G to purified viral antigen but did correlate with decreased proliferation of T lymphocytes to virus and myelin antigens. Silica quartz dust, a direct toxin of macrophages, suppressed demyelination and inflammation if begun at time of virus infection. No therapeutic effect was seen with inhibitors of plasminogen activators or other neutral proteases found primarily in macrophages.
J Neuroimmunol 1986 Dec
PMID:Effect of cyclosporin A, silica quartz dust, and protease inhibitors on virus-induced demyelination. 302 45

The early history of experimental allergic encephalomyelitis is reviewed from the point of view of the characterization and recognition of myelin basic protein and the active agent in acid-fast bacilli, namely muramyl dipeptide. Protocols effective in inducing demyelination are pinpointed. Special attention is paid to the protocol which depends on pretreating guinea pigs with muramyl dipeptide and foreign protein followed by a second injection of foreign protein and then the animals are injected with myelin basic protein and Freund's complete adjuvant. Variations in the timing and amounts of muramyl dipeptide are described as are their effects on the demyelination. The myelin breakdown has been studied with a monoclonal antibody reactive to P2. Similar pretreatment enhances the demyelination in Semliki Forest virus infection in mice. The changes in the blood brain barrier are found at 7 days after the myelin basic protein is injected and show grossly increased uptake by the cerebral vascular endothelium of IgG and perivascular uptake of IgG. The changes in the cerebrospinal fluid (CSF) proteins are described (IgG and albumin). Studies of P2 protein in the CSF by means of a new ELISA technique have been performed on human CSF in multiple sclerosis.
Brain Behav Immun 1988 Dec
PMID:Immunological and cytological studies of autoimmune demyelination and multiple sclerosis. 307 85


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