Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the functional role of the I region-associated (Ia) antigen in autoimmune central nervous system disorders, we generated long-term cultured lines of encephalitogenic T cells responsive to myelin basic protein from SJL strain mice (H-2s) and investigated genetic restriction in proliferative and encephalitogenic activities of the lines. These cell lines bear a Lyt 1+,2- phenotype, and show antigen-specific and I-As restricted proliferative responses in vitro. These lines induced full-blown experimental allergic encephalomyelitis (EAE) in immuno-compromised recipients carrying the I-As genotype. These data demonstrate that encephalitogenic T lymphocytes recognize the antigen in combination with the Ia antigen to induce EAE.
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PMID:Ia restriction of murine encephalitogenic T-cell lines in vitro and in vivo. 241 Apr 53

A series of 6 cases is described in which a chronic demyelinating neuropathy was associated with a relapsing multifocal CNS disorder, the clinical features of which resembled multiple sclerosis. Multifocal CNS lesions were demonstrated by CT and MR imaging and the presence of CNS demyelination was indicated by prolonged central conduction times. These cases are discussed in relation to the occurrence of combined peripheral and central demyelination in chronic relapsing experimental allergic encephalomyelitis and neuritis.
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PMID:Chronic demyelinating peripheral neuropathy associated with multifocal central nervous system demyelination. 302 54

Using murine monoclonal antibodies to mark total T cells, we have found rapid migration of T cells into the CSF in progressive multiple sclerosis patients, suggesting that the ongoing inflammatory responses in the CNS may depend on the continued movement of cells from the periphery into the target organ. Cloning experiments have indicated that the T cells present in the CSF during viral and post-viral encephalomyelitis represent sequestered populations of antigen-specific cells. In more chronic disease processes, these cells may also have restricted clonality as measured by the frequency of different T-cell receptor gene rearrangements on Southern blotting. It is known that there is restricted clonality of the B-cell immunoglobulin response in the CSF compartment with inflammatory CNS diseases, and with infections the majority of these so-called oligoclonal antibodies are directed against the exciting antigen and are synthesized in the CNS. Although we believe that T cells in the CNS originate from the blood, during the course of an inflammatory response the antigen and clonally-restricted populations found in the CSF may represent either selective migration or selective accumulation in the CNS. Selective migration might occur at the endothelial barrier as these cells can express Class II MHC antigens and act as antigen-presenting cells in the CNS (McCarron et al. 1985). Selective accumulation of T cells in the CNS might occur after non-specific migration of cells into the CNS followed by proliferation and expansion of T cells that have been induced by antigens in the brain. Antigen-presenting cells that are present in situ, such as astrocytes, may also play a role in the selective expansion of T cells in the CSF (Fontana et al. 1984). Alternatively, it is possible that T cells are induced to expand in the target CNS tissue non-specifically, e.g., via the CD2 pathway. In this regard, we have observed that CSF T cells exhibit alterations in stimulation by anti-T112 + anti-T113 monoclonal antibodies. The mechanism of damage to CNS tissue by immune cells is essentially unknown. For example there are no clear links between antibodies present in the CNS and CNS damage in SSPE where high titers of anti-measles antibodies are present. Whereas we did not observe high frequencies of measles-reactive cells in the CSF of a subject with SSPE, we did observe MHC non-restricted cytotoxic T cells which expressed TCR-gamma chains rather than alpha-beta chains.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:T cells in multiple sclerosis and inflammatory central nervous system diseases. 332 24

In recent years, herpes simplex virus has been recognized as an important CNS pathogen in neonates and adults. The recent development of effective antiviral therapy has substantially reduced the excessive morbidity and mortality associated with these infections. For neonatal herpes simplex infections, the current drug of choice is vidarabine. The results of ongoing clinical trials comparing vidarabine with acyclovir in neonatal herpes may lead to a change in the recommended therapy. In the adult, the therapy of choice for herpes simplex encephalitis is acyclovir. Although effective, the present therapies for herpes simplex infections of the CNS leave much room for improvement. In addition to the development of more effective antiviral drugs and less invasive diagnostic techniques, prevention of these often devastating infections will be important in reducing morbidity and mortality. The CNS diseases associated with varicella and herpes zoster may have a different pathogenesis. The implication for therapy in these diseases favors nonspecific supportive therapy in the varicella-associated syndromes. The few anecdotal reports of the use of vidarabine and acyclovir in herpes zoster encephalitis and the histopathologic evidence suggesting viral invasion of the CNS in many cases of zoster-associated neurologic syndromes makes the use of specific antiviral therapy in zoster encephalomyelitis more rational. However, appropriate therapeutic recommendations will have to be based on controlled clinical trials that have not yet been performed.
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PMID:CNS diseases associated with varicella zoster virus and herpes simplex virus infection. Pathogenesis and current therapy. 352 4

Establishment of animal model of virus-induced encephalomyelitis was attempted in strain 13 guinea pigs sensitized with the homologous spinal cord antigen. Intracerebral inoculation of canine distemper virus alone or sensitization with the neural antigen alone did not induce significant clinical signs. Mild histological lesions were found in both the meninges and parenchyma of the central nervous system (CNS) of virus-infected animals, and in the meninges of the sensitized ones. In contrast, combination of virus infection and sensitization resulted in development of neurological signs of CNS disease as well as of marked histological lesions involving both the meninges and parenchyma. The potentiated CNS disease was successfully transferred by the lymph node cells of the sensitized animals into virus-infected ones. These results suggested that the virus-induced lesions in the CNS were potentiated by the lymphocytes sensitized with neural antigen. Depending on the time schedule of the sensitization and virus infection, different courses of CNS diseases including acute, subacute, and/or recurrent ones were induced, indicating the usefulness of this animal model for immunological and virological analysis of virus-induced CNS diseases.
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PMID:Potentiation of neurovirulence of canine distemper virus in guinea pigs by sensitization with neural antigen. 617 11

Serological examinations of blood sera from patients with multiple sclerosis (MS), their nearest relatives, and subjects of the control groups for antibodies to causative agents of some viral infections demonstrated antihemagglutinins to measles and rubella viruses in 61%-95.5% of the subjects examined in all the groups, to mumps virus in 53% in MS patients, to tick-borne encephalitis virus in 2.2% in the same group, and in 10.5% in the group of patients with other CNS diseases, and none in healthy subjects. Virus-neutralizing antibodies to human acute encephalomyelitis virus (HAEM) in 28% of the cases, frequently in the stage of remission. Specific IgM to measles virus was found in 41% of MS patients, in 15% of their nearest relatives, and in 19.7% of patients with other CNS diseases, but not in healthy subjects. No differences in the rate of antibody findings to herpes simplex virus types 1 and 2 were observed in the groups examined. The rate of detection of virus-neutralizing antibody to HAEM virus was significantly higher in MS patients with the severity of the course of IV-V degree (20%) than of the II-III degree (8.8%). In the period of MS exacerbation the level of specific IgM to measles virus increased (35.6%), and higher titres of antihemagglutinins were observed in patients with longer duration of the disease and higher degree of its severity.
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PMID:[Detection of antibodies to the causative agents of viral infections in multiple sclerosis patients]. 684 21

Three weeks after a mild and presumably infectious illness, a 21-year-old man developed a CNS disorder characterized by involvement of the cerebellum, cerebrum, and brainstem. It progressed, sometimes stepwise, without remission, over five months to being bedfast with total spastic paraplegia, severe ataxia, and unintelligible dysarthric speech. The CSF showed increased levels of protein, IgG, and myelin basic protein, as well as five oligoclonal bands. Because of failure of the patient's condition to respond to prolonged prednisone therapy, poly ICLC was given intravenously weekly for 20 weeks (median dose, 100 microgram/kg). Improvement, evident after the first dose, progressed to the point of ambulation with some assistance. Even though the relation of the patient's marked recovery to poly ICLC therapy remains unproved, this experience provides reason for considering a possible therapeutic role of the drug in postinfectious demyelinating encephalomyelitis and perhaps in multiple sclerosis.
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PMID:Poly ICLC in the treatment of postinfectious demyelinating encephalomyelitis. 723 70

The medical records of 220 dogs with inflammatory/infectious diseases of the central nervous system (CNS) were retrospectively examined. The aims of the study were to determine if clinical and clinicopathologic data (not including biopsy or necropsy examination) could distinguish inflammatory CNS diseases from diseases of other types, and to search for criteria allowing differentiation of specific inflammatory diseases. The signalment, historical findings, extraneural and neurological signs, and the lesion site contributed marginally to a specific diagnosis. Multifocal signs were only noticed in one third of the dogs with inflammatory/infectious diseases. Particular neurological abnormalities were more frequent in certain diseases than in others (eg, myoclonus was frequent in dogs with distemper, but it was also found in those with other meningoencephalomyelitides). Hematologic findings contributed to the diagnosis in certain conditions (eg, canine distemper encephalitis, protozoal encephalomyelitis, steroid-responsive meningitis-arteritis). Cerebrospinal fluid examinations, including immunoglobulin G index and cytology were useful to separate meningoencephalomyelitides from the other CNS diseases and to distinguish certain conditions from others. In most cases a specific diagnosis depended on a combination of clinical signs and ancillary diagnostic aids. Still, a specific diagnosis remained very difficult, if not impossible, in at least one third of the dogs.
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PMID:Diagnosis of inflammatory and infectious diseases of the central nervous system in dogs: a retrospective study. 853 Nov 75

Paraneoplastic encephalomyelitis developed as the presenting feature of small-cell lung carcinoma in 3 patients. Two patients with paraneoplastic encephalomyelitis manifested predominantly as subacute sensory neuronopathy did not improve after prednisone treatment and chemotherapy. The third patient had severe axial and limb rigidity and myoclonus, which partially improved after chemotherapy and treatment with intravenous immunoglobulin and prednisone. Serum from each patient immunocytochemically stained the neuropil and to a lesser degree the neuronal cytoplasm in human cerebral and cerebellar cortex. On immunoblots of human neuronal extracts, each patient's serum contained high-titer IgG antibodies reacting with a protein band of apparent molecular mass 125 kd. This autoantibody pattern is indistinguishable from antibodies recently identified in several women with breast carcinoma and stiff-man syndrome. Screening of a human brain complementary DNA expression library with patient serum yielded clones whose sequence is identical to that of the synaptic vesicle-related protein amphiphysin. Reverse transcriptase-polymerase chain reaction demonstrated expression of amphiphysin in 8 of 10 small-cell lung carcinomas and in 5 of 14 breast carcinomas. These observations highlight the clinical and serological heterogeneity of paraneoplastic central nervous system disorders: Patients with a given clinical syndrome may have different antineuronal antibodies, and patients with a given autoantibody specificity have differing clinical presentations.
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PMID:Antiamphiphysin antibodies with small-cell lung carcinoma and paraneoplastic encephalomyelitis. 861 52

Experimental allergic encephalomyelitis (EAE) in macaques is an acute inflammatory and demyelinating disease of the central nervous system (CNS) which has been studied extensively as a model of the human demyelinating disease multiple sclerosis (MS). The in vivo administration of monoclonal antibodies against CD18, the common beta-chain of a leukocyte integrin, at the onset of clinical disease, significantly prolonged the survival of nine of 11 macaques (82%) and in some cases completely reversed the clinical appearance of disease. Treatment with anti-CD18 mAbs dramatically reduced the extent of inflammation in brain lesions as determined by magnetic resonance imaging (MRI). These improvements confirm that anti-CD18 mAbs are powerful anti-inflammatory agents in vivo and suggest that such mAbs may provide effective treatment of both demyelinating and inflammatory CNS diseases in man.
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PMID:Resolution of CNS lesions following treatment of experimental allergic encephalomyelitis in macaques with monoclonal antibody to the CD18 leukocyte integrin. 906 16


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