Disease relevance of Neuritis, Autoimmune, Experimental

• We have investigated the functional role of very late antigen-4 [VLA-4 (alpha4/beta1) integrin] and vascular cell adhesion molecule-1 (VCAM-1) in experimental autoimmune neuritis (EAN), an animal model of the Guillain-Barré syndrome, using neutralizing monoclonal antibodies (mAbs) as probes [1].
• Dominance of autoreactive T cell-mediated delayed-type hypersensitivity or antibody-mediated demyelination results in distinct forms of experimental autoimmune neuritis in the Lewis rat [2].
• TNF-alpha has been implicated as a potentially detrimental cytokine in autoimmune disorders of the nervous system and has been reported to be elevated in antigen-specific therapy of experimental autoimmune neuritis (EAN) in vivo [3].
• We have previously shown that cyclic AMP (cAMP)-elevating agents decrease the demyelination and Wallerian degeneration in experimental allergic neuritis [4].
• Rolipram suppresses experimental autoimmune neuritis and prevents relapses in Lewis rats [5].

High impact information on Neuritis, Autoimmune, Experimental

• When examined for effects in vivo, CP reduced clinical signs of inflammation in three T cell-mediated disease models including adjuvant-induced arthritis, experimental allergic neuritis, and cyclophosphamide-induced diabetes in NOD/Lt(F) mice [6].
• Transfer of demyelination by intraneural injection of experimental allergic neuritis serum [7].
• Since P2 protein is the antigen responsible for the induction of experimental allergic neuritis, these findings identify a potential mechanism involved in the inflammatory reaction and myelin damage during experimental allergic neuritis [8].
• We investigated by immunohistochemistry the expression of a number of integrin subunits during the course of experimental autoimmune neuritis (EAN) [9].
• Astrocytes upregulate glial fibrillary acidic protein (GFAP), but not insulin-like growth factor-I (IGF-I) during experimental autoimmune neuritis (EAN) [10].

Chemical compound and disease context of Neuritis, Autoimmune, Experimental

• By contrast, in rats immunized with bovine nerve root myelin, prednisolone at 10 mg/kg reduced the severity and duration of experimental allergic neuritis (EAN), the putative animal model for AIP [11].
• Suppression of experimental autoimmune neuritis by leflunomide [12].
• The neurotrophic analogue of ACTH(4-9), Org 2766, protects against experimental allergic neuritis [13].
• The role of macrophages and eicosanoids in the pathogenesis of experimental allergic neuritis. Serial clinical, electrophysiological, biochemical and morphological observations [14].
• Phosphatidylserine suppresses myelin-induced experimental allergic neuritis (EAN) in Lewis rats [15].

Biological context of Neuritis, Autoimmune, Experimental

• 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 [16].
• Blockade of signaling via the very late antigen (VLA-4) and its counterligand vascular cell adhesion molecule-1 (VCAM-1) causes increased T cell apoptosis in experimental autoimmune neuritis [17].
• To investigate whether the phosphorylation of extracellular signal-regulated kinase (ERK) is involved in autoimmune injury of the peripheral nervous system (PNS), the expression of phosphorylated ERK (p-ERK) was analyzed in experimental autoimmune neuritis (EAN) in rats [18].

Anatomical context of Neuritis, Autoimmune, Experimental

• Serial 1-micron-thick cryosections of ventral roots of animals with experimental autoimmune neuritis were labeled with Ox6 antibody against rat Ia, the ED1 antibody to identify monocytes/macrophages and an antiserum against S100, a marker for Schwann cells [19].
• Ia-positive structures were invariably negative for S100 at early and late stages of experimental autoimmune neuritis, indicating that Schwann cells did not express identifiable Ia antigen [19].
• Furthermore, FasL-expressing SC could be revealed by immunostaining of sciatic nerve from Lewis rats suffering from experimental autoimmune neuritis (EAN) [20].
• 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 [16].
• Suppression of experimental autoimmune neuritis by ABR-215062 is associated with altered Th1/Th2 balance and inhibited migration of inflammatory cells into the peripheral nerve tissue [21].

Gene context of Neuritis, Autoimmune, Experimental

• CCR5 deficiency does not prevent P0 peptide 180-199 immunized mice from experimental autoimmune neuritis [22].
• Monocyte chemoattractant protein 1 and chemokine receptor CCR2 productions in Guillain-Barré syndrome and experimental autoimmune neuritis [23].
• Involvement of cyclooxygenase-1 and -2 in the sciatic nerve of rats with experimental autoimmune neuritis [24].
• IL-10 suppresses experimental autoimmune neuritis and down-regulates TH1-type immune responses [25].
• Induction of experimental autoimmune neuritis with peripheral myelin protein-22 [26].

Analytical, diagnostic and therapeutic context of Neuritis, Autoimmune, Experimental

• Enhancement of acute phase and inhibition of chronic phase of experimental autoimmune neuritis in Lewis rats by intranasal administration of recombinant mouse interleukin 17: potential immunoregulatory role [27].
• Antigen-specific immunosuppression: nasal tolerance to P0 protein peptides for the prevention and treatment of experimental autoimmune neuritis in Lewis rats [28].
• In this study, using the quantitative competitive reverse transcriptase PCR method, we analyzed sequential expression of certain chemokine mRNAs in the cauda equina (CE) of rats with experimental allergic neuritis (EAN) [29].
• This study shows by Northern blot analysis that during experimental allergic neuritis (EAN), at the beginning of clinical signs, there is a transient extensive iNOS mRNA induction in nerve roots, in which morphology is mainly characterized by severe demyelination, but not in sciatic nerve, where scattered axonal degeneration is evident [30].
• Systemic complement depletion reduces inflammation and demyelination in adoptive transfer experimental allergic neuritis [31].

References