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

Experimental allergic encephalomyelitis (EAE) was induced by adoptive transfer of myelin basic protein (MBP)-activated LEW spleen cells into (LEW x PVG/c) F1----LEW chimeras. By double-immunofluorescent staining using OX27, which is specific for RT1c, and monoclonal antibodies (mAb) against various T-cell antigens (TAg), inflammatory cells in the lesions of the central nervous system (CNS) were categorized into MBP-activated and transferred LEW T cells (TAg+ OX27-), accompanying T cells (TAg+ OX27+) of chimera origin and non-T cells (TAg- OX27+). Examination of the lesions at various stages of EAE revealed that transferred OX19 (CD5)+ T cells accounted for 46% of the total number of inflammatory cells at the preclinical stage, became reduced to 23% at the clinical stage and recovered to a level between those of the preclinical and clinical stages at the recovery stage. In parenchymal infiltrates, 93% of the total T cells were transferred cells at the preclinical stage, whereas 66% were present in perivascular aggregates. At the clinical stage, the proportion of transferred T cells in the parenchyma was not different from that in the perivascular cuffs. At the recovery stage, the proportion of transferred T cells in the parenchyma was increased. Collectively, MBP-activated and transferred T cells first appeared in the CNS parenchyma followed by infiltration of T and non-T cells of recipient (chimera) origin. All these inflammatory cells formed the lesions of full-blown EAE. At the recovery stage, inflammatory cells decreased in number in all the compartments of the CNS. Transferred T cells formed the major proportion of parenchymal infiltrates at this stage. These findings strongly suggest that transferred T cells remain in the CNS parenchyma longer than cells of chimera origin and that antigen-activated T cells have well-expressed CNS-homing activity.
Immunology 1988 Sep
PMID:Adoptively transferred experimental allergic encephalomyelitis in chimeric rats: identification of transferred cells in the lesions of the central nervous system. 305 24

We have previously shown that astrocytes produce and secrete plasminogen activator (PA) and that this function is responsive to various modulating agents. When astrocyte conditioned medium (CM) is subjected to SDS-PAGE and PA activity localized by fibrin-agar gel overlay, the activity in the CM is found to comigrate with control t-PA. On affinity chromatography CM PA specifically binds to t-PA antibody. The latter also inhibits fibrinolytic activity of CM PA. When incubated with a fibrin clot, CM PA activity can be shown to bind to fibrin. These observations help identify the enzyme in astrocyte CM as t-PA. A possible role of astrocyte PA in myelin injury could provide an explanation for the previously observed correlation between fibrin deposition and demyelination as well as inhibition of demyelination by ancrod and heparin in experimental allergic encephalomyelitis.
J Neurol Sci 1987 Sep
PMID:Characterization of astrocyte plasminogen activator. 311 79

The vertebrate central nervous system (CNS) has been traditionally thought to be inaccessible for the passenger lymphocytes of the immune system. This does not seem to be the case: activated T-lymphocytes can readily cross the endothelial blood-brain barrier (BBB) and some glial cells, notably the astrocytes, seem to be programmed to act as most efficient and complex partners for antigen-specific T-lymphocytes. We used myelin basic protein (MBP) specific permanent rat T-lymphocyte lines as probes to assess the immune status of the CNS. These cells, upon activation in vitro, are able to transfer lethal, experimentally induced autoimmune-encephalomyelitis (EAE) to normal syngeneic recipients. Activated T-lymphocytes, but not resting ones, can break through the BBB irrespective of their antigen specificity. Immune surveillance of the CNS thus seems to be executed by activated T-lymphocytes. Having crossed the BBB, the activated T-cells interact with local glial cells by releasing factors, including interferon-gamma, which induced astrocytes to synthesize and express, on their membranes, class II major histocompatibility antigens (Ia determinants), which are critically required for immunogenic presentation of antigens to T-cells. Indeed, Ia-induced astrocytes of the CNS (and the Schwann cells of peripheral nerves) are efficient antigen presenter cells, which are able strongly to up-regulate antigen-reactive T-lymphocytes. In addition, it has recently been shown that at least some astrocytes are able to down-regulate immune cells. Some, but not all, astrocytes are capable of suppressing activation of T-cells. This suppression can be modulated by interferon-gamma, and is sensitive to irradiation. The question of whether suppression is mediated by direct cell-to-cell contact or via soluble mediators (e.g. apolipoprotein E) is under investigation. Astrocytes have been found to be most subtle regulators of immuno-competent T-cells. Most probably they are centrally involved in physiological immune reactivity of the CNS, and it will be tempting to learn how far glial cells are involved in transmitting regulatory signals between the immune and nervous systems.
J Exp Biol 1987 Sep
PMID:Immune reactivity in the nervous system: modulation of T-lymphocyte activation by glial cells. 332 5

The role of T-T cell interactions in the clinical course of acute experimental allergic encephalomyelitis (EAE) in mice was investigated. Myelin basic protein (MBP)-reactive and encephalitogenic T cell clones were established from long-term lines derived from susceptible strain SJL/J mice and resistant strain DDD/1 mice. The lines and clones from DDD/1 mice were obtained by immunization of congenitally athymic mice of DDD/1 origin, which had been reconstituted with syngeneic Lyt-2+-depleted splenic T cells. The clones derived from both strains bore surface phenotypes of Lyt-1+, 2- and L3T4+, and proliferated well in response to rat, rabbit, bovine, and guinea pig MBP in the presence of antigen-presenting cells with I-As. Passive EAE could be induced in syngeneic normal recipients by these clones as well as by the lines from which the clones were derived. The clinical features of the clone-induced EAE were essentially the same as those of the line-induced EAE. Furthermore, DDD/1 athymic recipients developed signs of acute EAE by the adoptive transfer of I-A-compatible syngeneic and allogeneic T cell clones, in which there was no significant difference in time of onset, maximum severity, or prognosis. These results indicate that the entire clinical course of acute EAE can be elicited by a single population of MBP-reactive T cells in the absence of the thymus and other populations of primed or unprimed T cells.
J Immunol 1986 Sep 01
PMID:Studies of experimental allergic encephalomyelitis by using encephalitogenic T cell lines and clones in euthymic and athymic mice. 348 35

The murine hepatitis virus, JHM strain, causes a relapsing subacute demyelinating encephalomyelitis in Lewis rats after intracranial infection. The disease process involves both virus persistence within glial cells and the induction of autoimmunological attack of myelin, however, the relative importance of these features involved in chronic relapsing demyelination remains to be determined. In this report, we analyze the tropism of JHM virus to various neural cell types present within primary Lewis rat central nervous system cultures. Infection of primary cultures with JHM virus revealed that type I astrocytes and brain macrophages are the initial target cells of infection and that the myelin-forming oligodendrocytes are comparatively resistant, becoming infected only rarely through virus mediated cell fusion with previously infected cells. In addition, infection of cultures after removal of oligodendrocytes by various means had no effect on the tropism of JHM virus for the cultures. Cytopathic effects of JHM virus proceed rapidly by cell fusion within the astrocyte-macrophage monolayer, leaving the oligodendrocyte population largely unaffected. Therefore, the highly selective infection of type I astrocytes and macrophages appears to form the basis of JHM virus neurotropism in Lewis rats. These results indicate that JHM virus infection of astrocytes and brain macrophages may be more important in inducing chronic relapsing demyelinating processes than direct infection of the myelin-forming oligodendrocytes. Other possible pathways leading to chronic demyelination in rats involving type I astrocytes and brain macrophages are discussed.
Lab Invest 1986 Sep
PMID:Analysis of murine hepatitis virus (JHM strain) tropism toward Lewis rat glial cells in vitro. Type I astrocytes and brain macrophages (microglia) as primary glial cell targets. 352 62

A heterotopic transplant paradigm was developed for its potential usefulness in dissecting genetically determined immune and central nervous system (CNS) components in the induction of experimental allergic encephalomyelitis (EAE). EAE is a cell-mediated, organ-specific, autoimmune disease producing inflammatory demyelination in the CNS. Susceptibility to EAE is determined by multiple genes and reflects both immune competence and target tissue responses. Syngeneic fetal CNS was heterotopically transplanted into the anterior chamber of the eye or beneath the capsule of the kidney of adult SJL or (SJL X BALB/c)F1 mice. Transplants usually survived better in the eye than the kidney. Six to eight weeks after transplantation, some mice were immunized for EAE. Immunized mice developed clinical and pathological signs of EAE in 12 to 15 days. The placement of CNS tissue into the eye or kidney prior to immunization did not suppress induction of EAE. Transplants in either location, in immunized mice, manifested perivascular inflammation and demyelination similar to that seen in the host CNS. However, transplants in mice not immunized for EAE, but maintained an equal time period after transplantation, did not demonstrate these features. The ability to produce the specific pathologic lesions of EAE in CNS tissue transplanted outside the CNS allows the design of studies of the tissue localization of genetic restrictions to development of EAE.
Exp Neurol 1987 Sep
PMID:Heterotopic brain transplants in the study of experimental allergic encephalomyelitis. 362 16

It has been established in the experiments on rats resistant to encephalomyelitis that vitamin E deficiency promoted and thymaline administration prevented the onset of the disease. The experiments on guinea-pigs sensitive to encephalomyelitis have shown that the combined administration of alpha-tocopherol and thymaline prevented the development of the disease. The results obtained make it possible to suggest that the resistance to encephalomyelitis depends on the level of membrane antioxidant defense and the condition of T-cell immunity.
Biull Eksp Biol Med 1987 Sep
PMID:[Effect of vitamin E and thymalin on the development of experimental allergic encephalomyelitis]. 366 10

In most demyelinating diseases, macrophages are believed to be active agents of myelin destruction. In experimental encephalomyelitis, these cells appear to strip off and ingest the myelin lamellae, and myelin debris has been observed within the cell body. We show here in vitro conditions in which rat peritoneal macrophages phagocytose and metabolize CNS myelin lipids. Purified rat myelin, prelabeled in vivo with [14C]acetate, was incubated with preimmune serum or rabbit antiserum to rat CNS myelin and added to macrophage monolayers. Myelin opsonized with antimyelin antibodies was more readily phagocytosed and metabolized by cultured macrophages than untreated myelin or that preincubated with preimmune serum. In the presence of macrophages, levels of myelin polar lipids and cholesterol decreased, whereas radioactive cholesterol ester and triglyceride accumulated. Up to five times as much radioactive cholesterol ester and about twice as much triglyceride accumulated in macrophage cultures containing antibody-treated myelin as in cultures fed preimmune serum-treated myelin or in those incubated with untreated myelin. Both the fatty acid and the cholesterol from cholesterol ester contained radioactive label; therefore, both were derived at least partly from the radioactive myelin lipid. Antiserum to myelin purified from peripheral nerve was almost as effective as that to CNS myelin in stimulating cholesterol metabolism, whereas antiserum to galactocerebroside was about 70% as active. Antiserum to basic protein had less effect, whereas antiserum to the myelin-associated glycoprotein and proteolipid protein was inactive. Of the polar lipids, ethanolamine phosphatide was most degraded in both the antiserum- and preimmune serum-treated myelin, with the diacyl form and plasmalogen form degraded about equally. These experiments indicate that myelin-specific antibodies in inflammatory CNS lesions may participate in and stimulate macrophage-mediated demyelination.
J Neurochem 1986 Sep
PMID:Opsonization with antimyelin antibody increases the uptake and intracellular metabolism of myelin in inflammatory macrophages. 373 1

Identification of the Negri bodies in the brain of an 8-year-old boy who died 8 days after a paralytic illness and 20 days after a dog bite, and who had received 9 injections of Semple's anti-rabies vaccine, provided evidence that he died of acute rabies encephalitis and not of post-vaccinal allergic encephalomyelitis. The Negri bodies in the human subject and those seen in the inoculated mouse differed in their morphological structure: the former consisted of a matrix of very fine granular material bearing larger granules or strands of higher electron-density resembling nucleic acids and representing products of host cell-virus interaction; and the latter showed better defined areas of granular matrix containing tubular, bullet-shaped and elongated forms of viral structures, and nucleocapsids or capsule-deficient cores, representing the virions, emerging from them. Fine structural examination of the patient's brain and of the inoculated mouse has provided evidence of the pleomorphism of the Negri bodies and the various stages of formation of viral material and virions in them, the animal alone showing the mature virions of rabies, and proving the infectivity of the Negri bodies of the human brain.
J Neurol Sci 1986 Sep
PMID:Pleomorphism of fine structure of rabies virus in human and experimental brain. 376 Sep 10

One-hundred-seventy-two serum samples, collected sequentially from four flocks of egg- and meat-type chickens, were evaluated for antibodies to multiple infectious agents by enzyme-linked immunosorbent assay (MELISA). The MELISA system used provided simultaneous measurement of antibody titers against avian infectious bronchitis (IB), infectious bursal disease (BD), Newcastle disease, avian encephalomyelitis and reovirus infections, and Mycoplasma gallisepticum. The use of computer-generated graphic print outs of relative MELISA titers provided immediate visulization of over 740 data points and convenient detection of any temporal changes in median titer class (MTC). The temporally changing MTC, or flock profiles obtained, indicated that negligible or waning IB immunity may be a common occurrence in previously vaccinated commercial chickens. These profiles further suggested that, despite no IB revaccination, these same flocks experienced episodes of reexposure to IB which otherwise may have been difficult to detect by conventional clinical or diagnostic laboratory protocols. MELISA profiles and sequential histologic examinations of bursas of Fabricius also provided evidence of a possible BD vaccination problem in young chickens that also experienced excessive losses from coccidiosis, ulcerative enteritis, and Marek's disease. Short sampling intervals were found to foster the detection and definition of fluctuations in MTC which otherwise may have been missed.
Poult Sci 1985 Sep
PMID:Presumptive diagnosis of subclinical infections utilizing computer-assisted analysis of sequential enzyme-linked immunosorbent assays against multiple antigens. 404 57


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