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PubMed1981

Prognosis of optic neuritis with special reference to cerebrospinal fluid immunoglobulins and measles virus antibodies.

Forty-eight patients with optic neuritis (ON), first seen in 1970 to 1973, were neurologically and neuroophthalmologically reexamined after 7 to 10 years. Twenty-seven patients (56%) had probable MS, and 9 (19%) had possible MS. During the attack of ON, the cerebrospinal fluid (CSF) samples and serum/CSF measles antibody ratios were studied. Twenty patients had increased relative immunoglobulin G (IgG) (% of total protein) in their CSF; 19 of these had probable or possible MS. However, 17 of 28 patients with a normal relative IgG value had also developed MS. CSF electrophoresis was abnormal in 20 patients with ON; reexamination showed that 19 had probable or possible MS. Sixteen of 27 patients with normal electrophoresis had also developed MS. Serum/CSF measles antibody ratio had decreased in 19 patients; 13 of these had probable MS and 3 had possible MS. Of 29 patients with a normal measles antibody ratio, 14 had probable MS and 6 had possible MS. The conclusion is that examination of the CSF in ON gives valuable prognostic information because increased relative IgG, abnormal electrophoresis, or a decreased measles antibody ratio implies a high risk of developing MS. A normal CSF does not, however, rule out the possibility of dissemination.

Antibodies, Viral↗

PubMed1984

The role of myelin P2 protein in the production of experimental allergic neuritis.

Myelin P2 protein has been proposed as the primary antigen in whole myelin-induced experimental allergic neuritis (EAN). We investigated the neuritogenic properties of P2 by sensitizing Lewis rats with complete Freund's adjuvant (CFA) containing P2, P2 plus phosphatidyl serine, or whole myelin containing an equivalent amount of P2. Animals were examined using a battery of clinical, electrophysiological, immunological, and morphological methods. Myelin-immunized rats developed the characteristic features of EAN. P2-sensitized rats developed a similar but much less intense disorder. When rats were sensitized with P2 in the presence of phosphatidyl serine, however, they developed radiculoneuropathy that was indistinguishable from myelin-induced EAN. Inoculation with phosphatidyl serine plus complete Freund's adjuvant or complete Freund's adjuvant alone had no detectable effect on peripheral nerves. These studies demonstrate that sensitization of rats with a single myelin antigen, P2 protein, is sufficient to induce the clinical, electrophysiological, and neuropathological features of EAN.

Animals↗

PubMed1986

Conduction failure and nerve conduction slowing in experimental allergic neuritis induced by P2-specific T-cell lines.

P2-specific T cells (LiP2/A) mediate experimental allergic neuritis (EAN) in the Lewis rat after adoptive transfer to naive recipients. After a latent period of 4 days, injection of 2 X 10(6) line cells induced fulminant paraplegia and complete conduction failure in the peripheral nerves and roots, resembling acute axonal breakdown. Injection with 10(6) cells caused milder clinical signs, nerve conduction failure, and conduction slowing. Clinical and electrophysiological recovery from adoptively transferred EAN was nearly complete and its time course was inversely correlated to the initial severity of EAN. These findings suggest that EAN induced by the P2-specific T-cell line can lead to a profound and rapidly evolving nerve dysfunction in a dose-dependent fashion.

Animals↗

PubMed1988

Suppression of experimental autoimmune neuritis by the oxygen radical scavengers superoxide dismutase and catalase.

Macrophages have been implicated in myelin damage in experimental autoimmune neuritis (EAN). We examined a possible pathogenetic role of toxic oxygen species elaborated by macrophages in EAN by administering oxygen radical scavengers. Early treatment of rats with either catalase or superoxide dismutase (10,000 U/kg/day) protected animals from the development of EAN. Treatment delayed until there was clinical manifestation of EAN (day 13) still markedly attenuated the severity of the disease, as evidenced by clinical assessment, electrophysiological studies, and morphological observation. In cell culture, macrophages from sham-treated controls generated heightened oxidative metabolic responses indicating in vivo macrophage activation. Addition of catalase or superoxide dismutase abrogated or diminished chemiluminescence and production of reactive oxygen intermediates by macrophages ex vivo. Our findings underscore the importance of macrophages in EAN and provide evidence that, in this model, macrophage-derived reactive oxygen intermediates contribute to damage of the myelin sheath.

Animals↗

PubMed1990

T-cell and macrophage activation in experimental autoimmune neuritis and Guillain-Barré syndrome.

Evidence implicating cellular immune responses in the pathogenesis of experimental autoimmune neuritis (EAN) and Guillain-Barré syndrome (GBS) is reviewed. In EAN the decisive role of T-lymphocytes in the initiation of immune-mediated nerve damage has been firmly established by adoptive transfer experiments. Macrophages but not Schwann cells express major histocompatibility complex class II gene products in situ and hence may function as antigen presenters. Macrophages are crucial in the amplification and effector phase and damage the myelin sheath by phagocytic attack and release of inflammatory mediators such as toxic oxygen radicals, arachidonic acid metabolites, complement, or hydrolases. Macrophage activation in EAN is achieved by interferon-gamma. Attempts to detect specific sensitization of T-lymphocytes to nerve antigens in patients with GBS have so far been unsuccessful. However, circulating activated T cells can be found in patients with GBS, as evidenced by augmented expression of HLA-DR antigen, the transferrin receptor, and the interleukin-2 receptor on the surface of peripheral blood T cells, and by increased serum concentrations of interleukin-2 and the soluble interleukin-2 receptor. In addition, we present data indicating macrophage activation in GBS.

Humans↗

PubMed1990

Gangliosides offer partial protection in experimental allergic neuritis.

The effect of gangliosides on the clinical course of experimental allergic neuritis was tested in Lewis rats sensitized with bovine intradural root myelin in complete Freund's adjuvant. A mixture of bovine brain gangliosides (GM1, GD1a, GD1b, GT1b) was injected intramuscularly at a daily dose of 20 mg per kilogram of body weight, beginning 6 days after inoculation. The results from seven different experiments show that in most cases, the administered gangliosides were partially protective. Particularly striking was the reduction in mortality rate to half or less of saline-injected controls. Cumulative clinical index scores were also significantly lower with ganglioside treatment in five of the seven experiments. The cause of the wide variability is not known, but it was noted that better results were obtained when the animals were sensitized with freshly isolated myelin.

Animals↗

PubMed1996

Bilateral brachial plexus neuritis following parvovirus B19 and cytomegalovirus infection.

A man, 23 years of age, had a typical erythema infectiosum, complicated by a severe bilateral brachial plexus neuritis. Motor function recovered slowly and only partially after 6 months. An infection by human parvovirus B19 was demonstrated, with strongly positive and gradually declining IgM antibodies and viral DNA detectable in serum for more than 3 months. There was also clear evidence of a recent infection by cytomegalovirus. The interaction between these two viruses could be responsible for this rare and severe complication of common infections in this patient.

Adult↗

PubMed1998

Matrix metalloproteinases MMP-9 and MMP-7 are expressed in experimental autoimmune neuritis and the Guillain-Barré syndrome.

Matrix metalloproteinases (MMPs) are a family of enzymes that may be implicated in the pathogenesis of inflammatory demyelinating disorders such as multiple sclerosis. The present study investigated the expression of 92-kd gelatinase (MMP-9) and five other MMPs in sciatic nerve from Lewis rats with autoimmune experimental neuritis (EAN), an experimental model of the Guillain-Barré syndrome (GBS). Quantitative polymerase chain reaction analysis revealed an up-regulation of MMP-9 mRNA with peak levels concurrent with maximal disease severity. Increased mRNA expression was associated with enhanced enzyme activity, as detected by gelatin zymography. Immunohistochemically, MMP-9 could be localized primarily around blood vessels within the epineurium and endoneurium in diseased but not normal sciatic nerve. Among all other MMPs investigated, mRNA levels of matrilysin (MMP-7) were found to be up-regulated at the peak of the disorder, remaining at high levels throughout the clinical recovery phase of the disease. To apply these findings to human disease, sural nerve biopsies from GBS patients were examined. By using immunohistochemistry, positive immunoreactivity against MMP-9 and MMP-7 was noted and corroborated by demonstrating augmented mRNA expression in comparison with noninflammatory neuropathies. Furthermore, increased MMP-9 activity was detected by zymography. These findings indicate that 92-kd gelatinase and matrilysin are selectively up-regulated during EAN and expressed in nerves of GBS patients and thus may contribute to the pathogenesis of inflammatory demyelination of the peripheral nervous system.

Animals↗

PubMed1987

Transverse myelitis and optic neuritis in systemic lupus erythematosus: a case report with magnetic resonance imaging findings.

We describe a patient with systemic lupus erythematosus who developed transverse myelitis and optic neuritis. Magnetic resonance imaging showed the presence of an abnormal signal in a normal-sized spinal cord which corresponded to the patient's neurologic deficit. No abnormality was recognized in either optic nerve. Magnetic resonance may prove to be a useful imaging modality for the diagnosis of a transverse myelopathy in systemic lupus erythematosus.

Adult↗

PubMed1977

Experimental allergic neuritis induced by a basic neuritogenic protein (P1L) of human peripheral nerve origin.

Experimental allergic neuritis (EAN) in the peripheral nervous system, without involvement of the central nervous system, was produced in laboratory animals by the injection of a basic neuritogenic protein, P1L, purified from human peripheral nerves. The animals manifested a positive skin test with P1L, and their lymphocytes were found to be transformed in vitro in the presence of this protein several days before the appearance of the clinical signs. Passive transfer of the disease was performed with lymph node cells from donor guinea pigs immunized with P1L protein. EAN, the experimental model for the human disease Guillaain-Barré syndrome, was shown to be a transient disease and could be suppressed by the administration of hydrocortisone.

Animals↗

PubMed1992

Cell adhesion molecules of the immunoglobulin supergene family as tissue-specific autoantigens: induction of experimental allergic neuritis (EAN) by P0 protein-specific T cell lines.

The P0 glycoprotein is a homophilic cell adhesion molecule of the immunoglobulin supergene family which is responsible for maintaining the structure of compact internodal myelin in the peripheral nervous system (PNS). Utilizing a panel of synthetic P0 peptides two distinct T cell epitopes have been identified that can induce T cell-mediated experimental autoimmune neuritis (EAN) in the Lewis rat. One T cell epitope (amino acid residues 56-71), is located within the extracellular, immunoglobulin-like domain of P0, while the other disease-inducing T cell epitope (residues 180-199) is located within the proteins cytoplasmic carboxyterminal domain. The adoptive transfer of 10(6) CD4+ T line cells specific for either of these peptide antigens induced EAN in syngeneic recipients. However, while the pathogenic response induced by both peptide-specific T cell lines was identical, their epitopes differ markedly in their immunologic properties in vivo. In particular while the response to peptide p180-199 was immunodominant in animals immunized with either purified P0 protein or the native membrane-bound P0 protein in autologous rat peripheral nerve myelin, no response to peptide p56-71 was detected, indicating that this epitope is cryptic. This study provides the first experimental evidence that the immunoglobulin-like domains of members of the immunoglobulin supergene family can function as target autoantigens in T cell-mediated autoimmune disease.

Amino Acid Sequence↗

PubMed2003

Heterozygous null mutation of myelin P0 protein enhances susceptibility to autoimmune neuritis targeting P0 peptide.

Mice with a heterozygous null mutation in myelin protein zero (P0(+/-)) develop late-onset clinical paralysis associated with inflammatory pathology in the peripheral nerves. Although the development of this illness is known to require T cells and macrophages, little is understood regarding the immunological defect in the mice. Here we report that young P0(+/-) mice, free from clinical manifestations, have a defect in central tolerance to P0, and are more prone to induction of experimental autoimmune neuritis (EAN) by sensitization against P0(180-199 )peptide. Notably, we found that the P0 gene is transcribed in the thymus of wild-type and the P0(+/-) mice in an amount proportional to the gene dosage. We then replaced the thymus of wild-type mice with that of the P0-deficient mice and vice versa. Immunization of these mice with P0(180-199 )revealed that a lower thymic P0 transcript would be associated with the higher recall T cell response to P0(180-199), thus accounting for the higher susceptibility of the P0(+/-) mice to P0-induced EAN. These results imply that a heterozygous mutation in an autoantigen could cause defective central tolerance to the autoantigen. As such, autoimmune T cells may play some role in "genetic" diseases caused by a heterozygous gene defect.

Amino Acid Sequence↗

PubMed2004

An MHC anchor-substituted analog of myelin oligodendrocyte glycoprotein 35-55 induces IFN-gamma and autoantibodies in the absence of experimental autoimmune encephalomyelitis and optic neuritis.

Previous strategies to ameliorate experimental autoimmune encephalitis (EAE) include the treatment of autoreactive T cells with altered peptide ligands, which contain amino acid substitutions at TCR contact residues. We recently showed that a variant of myelin oligodendrocyte glycoprotein (MOG) 35-55 possessing low affinity for MHC (45D) induced anergy in MOG 35-55-specific T cells and reduced their encephalitogenicity upon adoptive transfer. Here we investigate the characteristics of the primary immune response to this MHC anchor-substituted peptide. Overall, we observed that immunization with 45D resulted in the production of IFN-gamma and anti-MOG 35-55 autoantibodies at levels similar to those of MOG 35-55-immunized mice with active EAE. However, no symptoms of clinical or histological EAE or overt histological optic neuritis were observed in 45D-immunized mice. Consistent with this finding, 45D-immunized mice did not exhibit CD4(+) infiltrates into the CNS. Therefore, MOG 35-55-specific precursors stimulated with a weak ligand (45D) mediate some EAE-associated effector functions but are unable to fully initiate the inflammatory process in the central nervous system that leads to clinical manifestation of EAE.

Animals↗

PubMed2003

Human herpesvirus 7-associated meningitis and optic neuritis in a patient after allogeneic stem cell transplantation.

A 9-year-old boy who received allogeneic stem cell transplantation began to vomit from day 10 after transplantation. In addition to vomiting, the patient had a fever (from day 26) and severe headache (from day 34). His cerebrospinal fluid (CSF) (day 41) demonstrated pleocytosis with an absence of leukemic cells. Although the patient's symptoms were resolved with further supportive care, abrupt onset of bilateral decreased vision occurred at day 54. He was diagnosed with bilateral optic neuritis, due to the presence of disc edema and redness. Concomitant with the occurrence of aseptic meningitis, the human herpesvirus 7 (HHV-7) antibody titer increased significantly in this patient. Although neither HHV-6 nor cytomegalovirus (CMV) DNA was detected in CSF collected at day 41, HHV-7 DNA was detected in the sample. Viral DNA was not detected in CSF collected at day 93.

Antibodies, Viral↗

PubMed1977

Acute optic neuritis: a virological study in relation to multiple sclerosis.

Previous ultrastructural examination of peripheral blood lymphocytes revealed the presence of intranuclear filamentous structures in multiple sclerosis (MS) and in some optic neuritis (ON) patients. The present investigation was undertaken in the attempt to correlate the presence of such structures with the etiology of ON and MS and possibly to demonstrate the viral origin of the filaments. Suitable virological and serological techniques were used to detect and isolate infectious agents from peripheral blood samples and body excretions of 12 monosymptomatic ON patients at their first acute attack. Nevertheless, any efforts to demonstrate the presence of a virus in these patients have been unsuccessful: no evidence of active viral infection was obtained by serological studies of serum and cerebrospinal fluid samples, nor could viral antigens or inclusions be observed by immunofluorescence and cytochemical analysis. Negative results were also obtained from studies performed in parallel on MS patients and various controls. The significance of the failure to isolate infectious agents from either ON and MS patients is discussed.

Acute Disease↗

PubMed2002

Initiation and development of experimental autoimmune neuritis in Lewis rats is independent of the cytotoxic capacity of NKR-P1A+ cells.

Natural killer (NK) cells are implicated in T cell-mediated autoimmune diseases. Experimental autoimmune neuritis (EAN) is a CD4+ T cell-mediated animal model of the Guillain-Barré syndrome in human. The role of NK cells in the initiation and development of EAN remains unclear. In the present study, we demonstrate that anti-NKR-P1A monoclonal antibody (mAb) treatment in vivo did not affect the initiation and development of clinical EAN in Lewis rats induced by immunization with peripheral nerve myelin P0 protein peptide 180-199 and Freund's complete adjuvant, as well as the proportion of NKR-P1A+ cells (including NK cells and NKT cells) in the spleen. Furthermore, inflammatory cell infiltrations and demyelination in the peripheral nervous system (PNS) and in vitro P0 peptide 180-199-specific splenocyte proliferation were not different in anti-NKR-P1A mAb-treated rats compared to the control antibody-treated rats. The cytotoxic activity of NKR-P1A+ cells, determined by NK cell-sensitive K562 cells as target cells, decreased markedly in anti-NKR-P1A mAb-treated rats, suggesting that decrease of the cytotoxic activities of NKR-P1A+ cells is not sufficient to alter clinical EAN, although NKR-P1A+ cells may participate in the pathogenesis of T cell-mediated autoimmune diseases, such as EAN, by the mechanisms that involve the release of cytokines.

Animals↗

PubMed2004

Biphasic form of experimental autoimmune neuritis in dark Agouti rats and its oral therapy by antigen-specific tolerization.

A new and biphasic form of experimental autoimmune neuritis (EAN) is described in dark agouti rats (DA rats) and is inducible by a single immunization with bovine peripheral nerve myelin (BPM) in complete Freund's adjuvant (DA-EAN). Animals develop a mild episode of disease; after recovery, 66-100% of the rats suffer from a more severe bout of EAN with paraparesis 25-30 days after immunization. By histology, DA-EAN is an inflammatory and demyelinating polyradiculoneuropathy virtually without axonal damage. Demyelination affects mainly spinal roots. This is also reflected by markedly increased F-wave latencies in nerve conduction studies of sciatic nerves. In sciatic nerves, inflammation and demyelination are found only focally and may be the histopathologic basis for conduction failure in some fibers. Immunologic investigations revealed stronger proliferative responses of DA than of Lewis rat lymph node cells to BPM and various peptides derived from the P2 protein. Proliferative and Th1-cytokine responses were particularly pronounced in spleen during the late phase of DA-EAN as compared to the monophasic EAN of Lewis rats. The data suggest that persistent lymphocyte proliferation with secretion of interferon (IFN)-gamma may be relevant for the relapsing course of DA-EAN whereas epitope spreading may explain the increased severity of the second bout of disease. The extended Th1 response in DA rats did not go along with a lack of downregulatory mechanisms, because the second DA-EAN attack was self-limited and splenocytes from DA rats produced considerable amounts of interleukin (IL)-10 and transforming growth factor (TGF)-beta. To substantiate further a functional immunoregulation in DA rats, we modulated DA-EAN by antigen-specific oral tolerization, which is known to involve active suppressor mechanisms. Preventive feeding of BPM in combination with cholera toxin (CT) induced a long-lasting resistance to DA-EAN. Even therapeutic administration of BPM or BPM/CT after onset of signs of disease significantly mitigated the further course of disease and prevented development of paraparesis. Because DA-EAN is easily inducible and leads consistently to relapses in most rats, it can be used for studies of immune factors that determine a relapsing course of autoimmunity. Furthermore, DA-EAN may serve as a model for relapsing inflammatory demyelinating polyneuropathies such as chronic inflammatory demyelinating polyneuropathy (CIDP) and for treatment studies. Our findings on effective prevention and therapy of DA-EAN by oral application of myelin/CT corroborate this form of immunomodulation as a treatment strategy for cell-mediated processes in chronic inflammatory neuropathies.

Administration, Oral↗

PubMed1993

Transforming growth factor beta expression in reactive spinal cord microglia and meningeal inflammatory cells during experimental allergic neuritis.

Experimental allergic neuritis (EAN), an inflammatory demyelinating disorder of the peripheral nervous system, is preceded and accompanied by a massive microglial reaction in the spinal cord which occurs in the absence of inflammatory cells infiltrating the cord parenchyma. Since transforming growth factor beta (TGF-beta) has been shown to play a beneficial role in experimental autoimmune disease and might be involved in the regulation of glial activity, we have investigated the expression of TGF-beta in EAN spinal cord and nerve root tissue. Adoptive transfer EAN was induced by the injection of neurotogenic T-cells specific for the P2 myelin protein. In normal spinal cord tissue, both TGF-beta 1 and TGF-beta 3 mRNA were constitutively expressed at low levels. Already 3 days following injection of P2-specific T-cells, TGF-beta 1 mRNA levels began to increase, peaked at day 6 at levels about tenfold above normal, and thereafter declined. TGF-beta 3 was induced even earlier with a sharp rise at day 3 and a peak fourfold above normal at day 4. In situ hybridization for TGF-beta 1 performed on spinal cord sections 6 days after injection of cells localized TGF-beta 1 mRNA to many nonneuronal cells with the typical morphology of microglia. In addition, TGF-beta 1 mRNA was observed in the meninges, and massive accumulation of signal was seen over inflammatory cells infiltrating the nerve roots. Our data indicate that TGF-beta 1 and -beta 3 are involved in regulating the glial response in EAN and that activated microglial cells might control their own activity state by expressing TGF-beta 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗