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At least 775 records · Page 43Linked to original sources
PubMed1988

Electrophysiological follow up of experimental allergic neuritis mediated by a permanent T cell line in rats.

Acute experimental allergic neuritis (EAN) was produced in Lewis rats by transfer of lymphocytes from a permanent T cell line specific for bovine P2 protein. In 3 groups of rats receiving 10(4), 10(5) and 10(6) total injected P2-specific lymphocytes, respectively, the time course of illness was followed by measuring several electrophysiological parameters including the H reflex or F wave and lumbospinal somatosensory evoked potentials (SEP). The severity and time course of both the electrophysiological and clinical (e.g., loss of weight and development of paresis) parameters of illness depended on the number of injected lymphocytes. Lower numbers of injected cells were correlated with a later onset and less severe symptoms as well as with an earlier and more complete recovery. According to clinical observation EAN mediated by lymphocytes is a monophasic illness. According to our electrophysiological measurements, however, the disease can be described by the following successive stages: (a) an early stage of hyperexcitability; (b) a stage of acute partial conduction block; (c) 14 days later a stage of maximal demyelination; and (d) a recovery phase. Although demyelination is the prominent feature of the disease, axonal degeneration also occurs to an extent directly related to the number of cells injected. Degeneration was not observed in rats from the group with the lowest number (10(4] of injected lymphocytes.

Animals↗
PubMed1988

Modulation of experimental allergic neuritis in rats by in vivo treatment with monoclonal anti T cell antibodies.

Monoclonal antibodies (MCA) to different T lymphocyte cell surface antigens have been used to treat rats during different phases of the development of experimental allergic neuritis (EAN). The effects of this treatment were followed by clinical evaluation and in some instances by immunohistochemical analysis of lymphoid organs and affected nerves of the antibody-treated rats. Several MCA, W3/13 (pan T cell reactive), W3/25 (anti-rat CD4), Ox 8 (anti-rat CD8) as well as Ox 6 (anti-Ia) partly prevented clinical signs of EAN when given shortly before expected onset of disease, whereas W3/13 and Ox 8 given at the height of disease did not further affect disease development. However, Ox 19 (anti-rat CD5) given at the same time as immunization partly prevented clinical signs of EAN, while Ox 19 given shortly before expected onset of disease or during height of disease drastically exaggerated disease symptoms. Immunohistochemical studies after Ox 8 or Ox 19 treatment showed a complete absence of staining for the respective antibodies, while staining was preserved with the other MCA. It is concluded that: (1) Ox 8 positive "suppressor/cytotoxic" T lymphocytes do not exert any suppressive effects on EAN during the now investigated phases of disease, and that (2) anti T lymphocyte antibodies (here Ox 19) may exert opposite effects on autoimmune disease when given at different phases of disease development. This may have implications for potential therapeutic trials of MCA therapy for putative autoimmune demyelinating diseases in man.

Animals↗
PubMed1988

An immunohistological study of autoimmune encephalomyelitis and neuritis in the rabbit. Observations in the dorsal root ganglion using the freeze-dried paraffin-embedded tissue technique.

Previous studies of experimental autoimmune encephalomyelitis have shown that, in the central nervous system, the emigration of T-lymphocytes precedes that of mononuclear phagocytes during inflammatory lesion formation. In the present report, the formation of analogous lesions of autoimmune neuritis (EAN) was investigated in the dorsal root ganglia of rabbits immunized with homologous spinal cord in Freund's adjuvant. The relative time course of emigration of T-lymphocytes and mononuclear phagocytes into the ganglia was examined using monoclonal antibody labeling of both types of cells in serial sections of freeze-dried paraffin-embedded tissue. Results indicate that, unlike in the central nervous system, in the rabbit dorsal root ganglion T-lymphocytes and mononuclear phagocytes appear to emigrate simultaneously, as revealed by their concomitant presence in the earliest detectable lesions of EAN. It was also found that the cortical region of the rabbit dorsal root ganglion was a preferential site of EAN lesion formation, and that such lesions correlated well with the onset of clinical signs of paralysis. These results are discussed within the context of known "blood-tissue barriers" and the possible local modulation of inflammatory cell entry into regions of the nervous system.

Animals↗
PubMed1989

Immunological studies on patients with optic neuritis without evidence of multiple sclerosis.

We studied 6 patients with idiopathic optic neuritis (ON) after a mean follow-up period of 12 years. No evidence of multiple sclerosis (MS) was found on clinical grounds, nor by magnetic resonance imaging (MRI) or evoked responses. Levels of spontaneous proliferation, serum gamma-interferon (IFN-gamma) and lymphocyte MHC locus II antigen were similar in ON and in 6 patients with progressive MS, but different in healthy controls. This suggests that similar immunological conditions in vivo prevail after an idiopathic ON and in MS. A normal PHA-induced interleukin-2 receptor expression and lymphocyte proliferation but a low IFN-gamma secretion and MHC locus II antigen expression were observed. This suggests that an ON and MS defect is expressed after an interleukin-2 receptor ligand but before IFN-gamma secretion. Our findings also suggest that immunological factors do not explain the neuropathological confinement of the lesions in ON but the protective influence may rather be exerted by some as yet undefined genetic influence or may be explained by the different etiology of ON and MS.

Adult↗
PubMed1992

Evaluation of IL-2, sIL2R, IL-6, TNF-alpha, and IL-1 beta levels in serum and CSF of patients with optic neuritis.

Optic neuritis (ON) is characterized by immune-mediated demyelination of the optic nerve. In this study we addressed the question of cytokine signalling as part of activation of the immune system. 20 patients with first episode of acute idiopathic unilateral ON, prolonged visual evoked potentials, but normal 1.5 tesla MRI of the brain, and normal somatosensory evoked potentials were included into the study. Paired cerebrospinal fluid (CSF) and serum samples of these patients were analyzed for the presence of interleukin (IL-)-2, soluble IL-2R (sIL2R), IL-6, tumor necrosis factor (TNF)-alpha, and IL-1 beta by an enzyme-linked immunosorbent assay (IL-2, sIL2R, TNF-alpha, IL-1 beta) or a bioassay (IL-6). IL-2 was significantly elevated in the CSF (P < 0.01), whereas sIL2R (P < 0.01) and IL-6 (P < 0.01) were significantly increased in serum. TNF-alpha could not be detected in CSF or serum, and IL-1 beta was negative in serum in all but one sample and positive in only low amount (mean 9 pg/ml) in the CSF of 6/20 patients. This cytokine pattern in ON indicates an activation of the immune system within and outside the central nervous system with a predominance of T-cell activation.

Adolescent↗
PubMed1993

Selective elimination of macrophages by dichlormethylene diphosphonate-containing liposomes suppresses experimental autoimmune neuritis.

The injection of liposome-encapsulated dichlormethylene diphosphonate (Cl2MDP) constitutes an effective method to selectively eliminate phagocytic cells from spleen, liver and the circulation. We evaluated the effect of Cl2MDP-liposomes on the course of actively induced and adoptively transferred experimental autoimmune neuritis (EAN), both animal models of the human Guillain-Barré syndrome. Injection of Cl2MDP-liposomes 11 and 13 days postimmunization (p.i.) of Lewis rats with bovine peripheral nerve myelin efficiently prevented clinical signs of EAN up to day 15 p.i., when all control animals were affected. Thereafter, EAN gradually also developed in Cl2MDP-liposome-treated rats, but until day 19 disease was significantly milder than in control rats injected with buffer-filled liposomes. Adoptive transfer EAN (AT-EAN) induced by injection of activated P2-specific T cells could be suppressed even more markedly by application of Cl2MDP-liposomes 1, 3, and 6 days after cell transfer. Efficient suppression of AT-EAN by Cl2MDP-liposomes rules out the possibility that EAN is prevented due to interference with the induction phase of this experimental disease and confirms that macrophages are important effector cells during EAN. Selective suppression of phagocytic cell function by drug-containing liposomes may hold promise as a novel treatment of demyelinating autoimmune diseases of the nervous system.

Animals↗
PubMed1993

Detection and quantification of antibodies to the extracellular domain of P0 during experimental allergic neuritis.

Quantification of the peripheral nerve myelin glycoprotein P0 and antibodies to P0 is difficult due to insolubility of P0 in physiological solutions. We have overcome this problem by using the water-soluble recombinant form of the extracellular domain of P0 (P0-ED) and describe newly developed assays which allow detection and quantitation of P0 and antibodies to P0, in serum and cerebrospinal fluid (CSF). These sensitive and specific assays based on the ELISA technique were used to study humoral immune responses to P0 during experimental autoimmune ("allergic") neuritis (EAN). In order to establish these tests, monoclonal antibodies to different epitopes of rodent and human P0-ED were produced. A two-antibody sandwich-ELISA allowing quantitation of P0 (lower detection limit of 0.5 ng/ml or 30 fmol/ml) and an antibody-capture ELISA (lower detection limit 1 ng specific antibody/ml) to detect antibodies to P0 in serum and CSF were developed. EAN was induced in rats by active immunization with bovine myelin or the neuritogenic protein P2 or by adoptive transfer using P2 specific CD4 positive T cells. Serum and CSF were assayed for the presence of P0-ED and antibodies to P0-ED or P2. Antibodies to P0-ED were detected during active myelin-induced EAN, but not during P2-induced or adoptive transfer EAN. The anti-P0-ED antibodies in the CSF showed a correlation with disease activity. In contrast, in the same model antibodies to P2 persisted long after the disease ceased. No soluble P0-like fragments could be found in serum or CSF during any of the three types of EAN. We conclude that P0 may be a B-cell epitope in EAN. These findings warrant a screen for antibodies to P0-ED in human immune neuropathies.

Animals↗
PubMed1994

The B cell repertoire in experimental allergic neuritis involves multiple myelin proteins and GM1.

Experimental allergic neuritis (EAN) is a T cell mediated disease associated with inflammation and demyelination of peripheral nerves. EAN is an experimental model of Guillain-Barré syndrome. The peripheral nerve myelin components P2 and P0 represent major neuritogens, but the diversity and quantity of B cell responses in EAN are unknown. Lewis rats were immunized with bovine peripheral nerve myelin (BPM), and levels of B cells secreting IgM and IgG antibodies to BPM, P2 and P0, the glycolipid GM1 and five peptides of myelin-associated glycoprotein (MAG) were determined. Already on day 7 post-immunization (p.i.), i.e. before the onset of clinical EAN, lymph nodes contained elevated levels of cells secreting IgM antibodies of all specificities examined. Maximum numbers of IgG antibodies secreting cells were generally reached at the height of clinical disease. The numbers of cells secreting IgG antibodies to BPM, P2, P0, GM1 and MAG peptides were also elevated before disease onset, but they were mostly higher than those of IgM antibodies and they reached their maximum only after recovery. The results imply that EAN is associated with strong B cell responses to all myelin antigens under study without restriction to any immunodominant myelin component or MAG peptides.

Amino Acid Sequence↗
PubMedDate not supplied

Neuro-ophthalmologic dilemma: chronic optic neuritis?

A patient with an 8-month history of chronic progressive visual loss was referred to the Neuro-ophthalmology Consult Office of Washington University with a diagnosis of chronic optic neuritis. Previous diagnostic studies, including CAT scan, had been negative. Because chronic progressive visual loss is considered a hallmark of mass lesion, more vigorous investigation, including repeat CAT scans, was undertaken, leading to the diagnosis and removal of a 2 cm meningioma.

Adult↗
PubMedDate not supplied

Optic neuritis--etiology?

A 44-year-old otherwise healthy woman was referred to Washington University with previous diagnoses of para planitis and retrobulbar neuritis, and with a current complaint of markedly decreased vision (light perception only) in the right eye. Among the findings at the time of this evaluation were posterior uveitis and evidence of optic neuropathy and of a disordered immune system. The patient responded to pulsed high-dose corticosteroid therapy. A subsequent similar episode in the left eye also was resolved with such treatment. Dr. Burde describes the case in detail and asks Drs. Keltner, Gittinger and Miller to offer diagnoses. Their answers vary considerably.

Adult↗
PubMedDate not supplied

What to tell the patient with optic neuritis about multiple sclerosis.

If the ophthalmologist tells the patient with an initial isolated attack of optic neuritis that multiple sclerosis may develop, will he/she worry the patient needlessly or provide useful information that the patient is rightfully entitled to have? In this set of articles, the philosophies and individual circumstances that should influence the ophthalmologist in deciding what information to supply are discussed.

Delivery of Health Care↗
PubMed1984

Association of CSF IgG concentration and immunoglobulin allotype in multiple sclerosis and optic neuritis.

The cerebrospinal fluid (CSF) and serum from 64 patients with multiple sclerosis (MS) and 47 patients with monosymptomatic optic neuritis (ON) were analyzed for the distribution of allotypic determinants on IgG and compared to similar samples from 51 patients with other neurological diseases (OND) as well as to serum samples from 97 healthy controls. The results indicate a significantly increased frequency of the haplotypes Gm a;g and Gm a,x;g among MS patients (P = 0.024) with an associated increase in relative risk for MS among individuals with the Gm a,(x);g haplotypes compared to those individuals without them (P = 0.014). Among MS patients, those with the Gm a,(x);g haplotypes had significantly higher CSF levels of IgG than those without (P = 0.016); levels of serum IgG did not covary with Gm haplotype. Two-way analysis of variance indicates that familial cases have significantly higher levels of CSF IgG than nonfamilial cases (P less than 0.001) and that familial cases with the Gm a,(x);g haplotypes have the highest CSF IgG levels (P less than 0.005). There was no correlation between Gm haplotype and CSF or serum IgG levels in patients with ON or OND. The allotype effects were independent of age at onset and duration of disease. In all patients, regardless of disease classification, the phenotypes found in serum samples were identical to those found in CSF samples. The data presented support the hypothesis that the etiology of MS has as one of its parameters an immunoregulatory/immunogenetic factor. The successful analysis of these various parameters will provide useful information not only about MS but also about general principles of human immune responsiveness.

Adolescent↗
PubMed1982

Protection against experimental allergic neuritis with silica quartz dust.

Lewis rats sensitized against peripheral nervous system antigens can be protected against experimental allergic neuritis (EAN) by the intraperitoneal injection of silica quartz dust. Two doses of 200 mg silica given 8 and 11 days post-inoculation (dpi) protected against the development of both clinical and pathological disease. A single dose of 200 mg silica 8 dpi gave significant protection against clinical disease but all animals developed pathological signs. A single injection of 200 mg silica 11 dpi, after the onset of early signs, protected against further progression of disease. The protection was long lasting. Given the known toxic effects of silica for macrophages, these results would support the conclusion that macrophages function during the effector stage in the clinical and pathological expression of EAN in the Lewis rat.

Animals↗
PubMed1982

Induction of allergic neuritis in rhesus monkeys.

Experimental allergic neuritis (EAN) was induced in rhesus monkey (Macaca mulatta) following sensitization with rabbit nerve (PNS) myelin in complete Freund's adjuvant (CFA) or with bovine P2 protein complexed with phosphatidyl serine (P2-lipid) in CFA. The response of monkeys receiving PNS myelin in CFA differed from the previous studies where monkeys developed clinical signs of fatal EAN within 15-20 days following sensitization. The monkeys in this study (6) showed a much longer delay (40-114 days) before the appearance of severe clinical signs, and 4 of the 6 animals survived without further attack (1 year). Monkeys (4) injected with P2-lipid (2:1 ratio; w/w) developed severe clinical signs of EAN which was fetal in 3 cases. Peripheral lymphocytes from monkeys sensitized to the P2-lipid showed a much stronger mitogeneic response to P2 protein than those from the PNS myelin-sensitized monkeys. on quantitation of the circulating anti-P2 antibodies, the P2-sensitized monkeys generally had much titers than those sensitized with PNS myelin.

Animals↗
PubMed1982

Antibodies to P2 and P1 myelin antigens in experimental allergic neuritis and allergic encephalomyelitis.

We confirmed earlier observations that experimental allergic neuritis (EAN) in Lewis rats induced by injection of bovine peripheral nerve myelin in complete Freund's adjuvant is not accompanied by development of experimental allergic encephalomyelitis. However, sera of these animals contained elevated titers of antibodies against central nervous system myelin basic protein (BP), likely induced by peripheral nerve P1 protein. Anti-BP antibodies were not seen in sera of rats with EAN induced by peripheral nerve P2 protein. Lack of encephalogenicity of bovine myelin in Lewis rats does not reflect simply lack of immune responses induced against BP.

Animals↗
PubMed1982

Involvement of autonomic nervous system in experimental allergic neuritis. A light- and electron-microscopic study.

The affection of the sympathetic and parasympathetic structures of the peripheral nervous system in rabbits with experimental allergic neuritis (EAN) was demonstrated light- and electron-microscopically. The general characteristics of the microscopic findings were qualitatively similar to those previously established in the somatic nervous system, but they were less extensive. The neuronal perikarya and the axons in the autonomic nervous system (ANS) were mostly normal. Occasionally, cytoplasmic vacuoles in a few nodose ganglion neurons and some degenerating axons were seen. Other than myelin derived antigens could be operating in whole-nerve induced EAN, since inflammatory cells also infiltrated target tissue areas devoid of myelinated nerve fibers. The presence of numerous plasma cells in the target tissue suggests that local antibody formation may contribute to the destructive process. Our results establish that the ANS is frequently affected in EAN, especially in the more severe forms. Thus EAN was proved to be also in this respect a useful model for the human disease Guillain-Barré syndrome, which likewise is often complicated by autonomic dysfunctions.

Animals↗
PubMed1983

Interferon-alpha and interferon-gamma production capacity of idiopathic isolated optic neuritis patients.

Interferon-alpha and interferon-gamma production by idiopathic isolated optic neuritis (ON) patients was studied. The production capacity was compared with that in two control groups: patients with iritis and healthy control subjects. A sensitive and reliable interferon bioassay was applied for interferon level measurements. Statistically significant differences were not found between patients and control groups in either interferon-alpha production or interferon-gamma production.

Adult↗
PubMed1984

Circulating lymphocyte subpopulations in experimental allergic neuritis.

T-cell subsets in the peripheral blood were analyzed using monoclonal antibodies during the development of experimental allergic neuritis in Lewis rats. Percentages of helper and suppressor cells and ratios of helper/suppressor cells did not exceed normal limits during the development of the disease.

Animals↗