The Inflammatory Lesion in Idiopathic Polyneuritis

Asbury, Arthur K.; Arnason, Barry G. W.; Adams, Raymond D.

doi:10.1097/00005792-196905000-00001

Cited by 686 publications

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“…At the same time there is a part of the PNS, particularly dorsal root ganglia and dorsal roots, where the blood microvessels are devoid of barrier properties (54) and which are in direct contact with the CSF in the subarachnoid cavity of the spinal cord. The pathomorphological picture of the GBS includes inflammatory infiltrates (a sign of the local activation of the immune system) around the peripheral nerve fibers, which mainly consist of lymphocytes and monocytes (7,55). In addition, in an animal model of the spontaneous autoimmune peripheral polyneuropathy (presymptomatic L31/CD4Ϫ/Ϫ mice), the infiltration of immune cells was noted precisely in the areas of the DRG and spinal roots prior to disease onset (56).…”

Section: Discussionmentioning

confidence: 99%

“…The development of experimental allergic neuritis (EAN) by injecting peripheral nervous tissue together with Freund's adjuvant into rabbits disclosed some similarities with the autoallergic symptoms of GBS, which finally allowed attributing this disease to neuroautoimmunity (6).. The autoimmune features of GBS were further supported by Asbury et al in their autopsy studies of GBS patients (7). More recently, precise cellular immunological and immunochemical studies of EAN models allowed researchers to partially uncover the mechanisms of GBS development and pathogenesis (8,9).…”

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confidence: 90%

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The Pathogenesis of the Demyelinating Form of Guillain-Barre Syndrome (GBS): Proteo-peptidomic and Immunological Profiling of Physiological Fluids

Ziganshin

Ivanova

Lomakin

et al. 2016

Molecular & Cellular Proteomics

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Acute inflammatory demyelinating polyneuropathy (AIDP) -the main form of Guillain-Barre syndrome-is a rare and severe disorder of the peripheral nervous system with an unknown etiology. One of the hallmarks of the AIDP pathogenesis is a significantly elevated cerebrospinal fluid (CSF) protein level. In this paper CSF peptidome and proteome in AIDP were analyzed and compared with multiple sclerosis and control patients. A total protein concentration increase was shown to be because of even changes in all proteins rather than some specific response, supporting the hypothesis of protein leakage from blood through the blood-nerve barrier. The elevated CSF protein level in AIDP was complemented by activization of protein degradation and much higher peptidome diversity. Because of the studies of the acute motor axonal form, Guillain-Barre syndrome as a whole is thought to be associated with autoimmune response against neurospecific molecules. Thus, in AIDP, autoantibodies against cell adhesion proteins localized at Ranvier's nodes were suggested as possible targets in AIDP. Indeed, AIDP CSF peptidome analysis revealed cell adhesion proteins degradation, however no reliable dependence on the corresponding autoantibodies levels was found. Proteome analysis revealed overrepresentation of Gene Ontology groups related to responses to bacteria and virus infections, which were earlier suggested as possible AIDP triggers. Immunoglobulin blood serum analysis against most common neuronal viruses did not reveal any specific pathogen; however, AIDP patients were more immunopositive in average and often had polyinfections. Cytokine analysis of both AIDP CSF and blood did not show a systemic adaptive immune response or general inflammation, whereas innate immunity cytokines were up-regulated. To supplement the widely-accepted though still unproven autoimmunity-based AIDP mechanism we propose a hypothesis of the primary peripheral nervous system damaging initiated as an innate immunity-associated local inflammation following neurotropic viruses egress, whereas the autoantibody production might be an optional complementary secondary process. Molecular & Cellular

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 90%

The Pathogenesis of the Demyelinating Form of Guillain-Barre Syndrome (GBS): Proteo-peptidomic and Immunological Profiling of Physiological Fluids

Ziganshin

Ivanova

Lomakin

et al. 2016

Molecular & Cellular Proteomics

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“…In patients with acute inflammatory demyelinating polyradiculoneuropathy (AIDP), which constitutes up to 70% of cases of GBS [7], histological studies of peripheral nerve taken at post-mortem typically show evidence of a lymphocytic infiltrate surrounding vessels [8,9]. The histological findings are similar to those of the animal model of GBS, experimental allergic neuritis (EAN) [10].…”

Section: Introductionmentioning

confidence: 98%

Stimulation of peripheral blood lymphocytes with Campylobacter jejuni generates a γδ T cell response in patients with Guillain–Barré syndrome

Ben-Smith¹,

Goodall

Gaston

et al. 1997

Clinical and Experimental Immunology

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SUMMARYIn three patients whose Guillain-Barré syndrome (GBS) was preceded by gastrointestinal infection due to Campylobacter jejuni, gd T cells were generated from peripheral blood in response to in vitro stimulation with C. jejuni. In one of the patients, where a diagnostic sural nerve biopsy was performed, gd T cells were also isolated following culture of the nerve tissue. Studies with healthy volunteers and C. jejuni gastroenteritis patients also showed preferential enrichment for gd T cells in peripheral blood cells stimulated with C. jejuni, although the response was significantly lower than that seen in GBS patients. In two out of three GBS patients and all of the controls, gd T cell receptor (TCR) gene usage was shown to be Vg9/Vd2 + . In the GBS patient where nerve-infiltrating gd T cells were isolated, these and C. jejuni-specific peripheral blood cells had similar TCR gene usage, predominantly consisting of Vg5/Vd1 + cells. Sequencing the Vd1 products from nerve and peripheral blood showed similarities in CDR3 length, but the single Vd1 sequence obtained from nerve was not identified in peripheral blood. These results suggest that the generation of gd T cells is part of a normal immune response to C. jejuni, which, in patients with GBS, may contribute to the pathogenesis of their inflammatory neuropathy.

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“…Experimental autoimmune neuritis (EAN) is a demyelinating inflammatory polyradiculoneuropathy that represents an animal model for understanding the mechanisms of acute and chronic inflammatory demyelinating polyradiculoneuropathy (AIDP or Guillain-Barré syndrome, GBS and CIDP) [1,2]. EAN can be induced by immunizing susceptible animals with peripheral nerve myelin [3], peptides [4] or by passively transferred with lymph node cells (LNC) [5].…”

Section: Introductionmentioning

confidence: 99%

Passive Transfer of Experimental Autoimmune Neuritis by IL‐12 and IL‐18 Synergistically Potentiated Lymphoid Cells is Regulated by NKR‐P1+ Cells

Sun

Wang

et al. 2007

Scand J Immunol

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The aim of this study was to investigate the roles and mechanism of interleukin‐12 (IL‐12) and interleukin‐18 (IL‐18) in potentiating the autoreactivity of lymphoid cells specific for P2 53–78 peptide. P2 53–78‐specific lymphoid cells in the presence of IL‐12 or IL‐18 alone passive transferred only moderate experimental autoimmune neuritis (EAN) into a low percentage of recipients. However, lymphoid cells co‐cultured with both cytokines transferred aggressive clinical and histological EAN into all recipients. NKR‐P1+ cells (including NK and NKT cells) played an immunosuppressive function in passive transfer EAN and depletion of NKR‐P1+ cells by anti‐NKR‐P1 Ab and complement induced a more serious form of EAN. Nevertheless, lymphoid cells co‐cultured with both IL‐12 and IL‐18 induced high levels of interferon‐γ (IFN‐γ) and promoted Th1 differentiation partially through NKR‐P1+ cells and to some extent, NKR‐P1+ cell depletion inhibited the auto‐reactivity of lymphoid cells treated with IL‐12 and IL‐18.

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The Inflammatory Lesion in Idiopathic Polyneuritis

Cited by 686 publications

References 0 publications

The Pathogenesis of the Demyelinating Form of Guillain-Barre Syndrome (GBS): Proteo-peptidomic and Immunological Profiling of Physiological Fluids

The Pathogenesis of the Demyelinating Form of Guillain-Barre Syndrome (GBS): Proteo-peptidomic and Immunological Profiling of Physiological Fluids

Stimulation of peripheral blood lymphocytes with Campylobacter jejuni generates a γδ T cell response in patients with Guillain–Barré syndrome

Passive Transfer of Experimental Autoimmune Neuritis by IL‐12 and IL‐18 Synergistically Potentiated Lymphoid Cells is Regulated by NKR‐P1+ Cells

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