Class II antigen expression in peripheral neuropathies

Mitchell, Gregory; Williams, G. Stuart; Bosch, E. Peter; Hart, M. N.

doi:10.1016/0022-510x(91)90065-f

Cited by 41 publications

(16 citation statements)

References 24 publications

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“…Cell surface levels of MHC Class I molecules can be elevated and expression of MHC Class II molecules can be induced by proinflammatory cytokines (Ansselin and Pollard, 1990; Bergsteinsdottir et al, 1992; Gold et al, 1995; Kingston et al, 1989; Lisak and Bealmear, 1992; Samuel et al, 1987; Tsai et al, 1991; Tsuyuki et al, 1998). HLA complexes have been visualized in human peripheral nerve sections (Mancardi et al, 1988; Mitchell et al, 1991; Pollard et al, 1987; Wanschitz et al, 2003), although data regarding expression of HLA molecules by human Schwann cells in inflammatory conditions are sparse and controversial (Schmidt et al, 1990). Coculture experiments demonstrated that rodent Schwann cells can present endogenous and exogenous antigen to lymphocytes (Argall et al, 1992a, b; Duan et al, 2007; Ford et al, 1993; Kingston et al, 1989; Lilje, 2002; Wekerle et al, 1986), thereby providing evidence for a functional relevance of Schwann cell‐derived MHC expression.…”

Section: Discussionmentioning

confidence: 99%

Expression of antigen processing and presenting molecules by Schwann cells in inflammatory neuropathies

Hörste

Heidenreich

Lehmann

et al. 2009

Glia

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Schwann cells are the myelinating glia cells of the peripheral nervous system (PNS) and can become targets of an autoimmune response in inflammatory neuropathies like the Guillain-Barré syndrome (GBS). Professional antigen presenting cells (APCs) are known to promote autoimmune responses in target tissues by presenting self-antigens. Other cell types could participate in local autoimmune responses by acting as nonprofessional APCs. Using a combined approach of immunocytochemistry, immunohistochemistry, and flow cytometry analysis we demonstrate that human Schwann cells express the antigen processing and presenting machinery (APM) in vitro and in vivo. Moreover, cultured human Schwann cells increase the expression of proteasome subunit delta (Y), antigen peptide transporter TAP2, and HLA Class I and HLA Class II complexes in an inflammatory environment. In correlation with this observation, Schwann cells in sural nerve biopsies from GBS patients show increased expression of antigen processing and presenting molecules. Furthermore, cultured human Schwann cells can proteolytically digest fluorescently-labeled nonmammalian antigen ovalbumin. Taken together, our data suggest antigen processing and presentation as a possible function of Schwann cells that may contribute to (auto)immune responses within peripheral nerves.

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Section: Discussionmentioning

confidence: 99%

Expression of antigen processing and presenting molecules by Schwann cells in inflammatory neuropathies

Hörste

Heidenreich

Lehmann

et al. 2009

Glia

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“…S100, PO, and NGFR staining identified the origin of abnormal cells in localized hypertrophic neuropathy (Sciacco et al, 1992); expression of MHC class I1 molecules in SC was measured in both non-inflammatory and inflammatory human neuropathies (Mancardi et al, 1988;Mitchell et al, 1991;Scarpini et al, 1990;Williams et al, 1992); and the expression of peripheral myelin protein 22 kd was measured in Charcot-Marie-Tooth IA hereditary neuropathies, in which PMP-22 gene dosage is likely to be pathogenetic (Hanemann et al, 1994;Yoshikawa et al, Fig. 3.…”

Section: Injured Rat Sciatic Nerve Predicts Sc Marker Expression In Hmentioning

confidence: 99%

β4 integrin and other Schwann cell markers in axonal neuropathy

Quattrini

Previtali

Feltri

et al. 1996

Glia

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“…A single study of 9 patients failed to demonstrate B-lymphocyte infiltration or complement and immunoglobulin deposits, while another study of 105 patients demonstrated C3d in 30% of patients without B-lymphocyte infiltration or immunoglobulin [82,115]. Increased expression of HLA-DR on monocytes/macrophages, Schwann cells, in capillary endothelial cells and within the perineurium in areas of active demyelination or remyelination in CIDP compared to basal expression on endothelial cells, very occasional mononuclear cells and sparsely within the perineurium in controls has been described [82,88,104]. …”

Section: Introductionmentioning

confidence: 99%

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Ubogu

2015

Acta Neuropathol

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Inflammatory neuropathies encompass groups of heterogeneous disorders characterized by pathogenic immune-mediated hematogenous leukocyte infiltration of peripheral nerves, nerve roots or both, with resultant demyelination or axonal degeneration or both. Inflammatory neuropathies may be divided into three major disease categories: Guillain-Barré syndrome (particularly the acute inflammatory demyelinating polyradiculoneuropathy variant), Chronic inflammatory demyelinating polyradiculoneuropathy and nonsystemic vasculitic neuropathy (or peripheral nerve vasculitis). Despite major advances in molecular biology, pathology and genetics, the pathogenesis of these disorders remains elusive. There is insufficient knowledge on the mechanisms of hematogenous leukocyte trafficking into the peripheral nervous system to guide the development of specific molecular therapies for immune-mediated inflammatory neuropathies compared to disorders such as psoriasis, inflammatory bowel disease, rheumatoid arthritis or multiple sclerosis. The recent isolation and characterization of human endoneurial endothelial cells that form the blood-nerve barrier provides an opportunity to elucidate leukocyte-endothelial cell interactions critical to the pathogenesis of inflammatory neuropathies at the interface between the systemic circulation and peripheral nerve endoneurium. This review discusses our current knowledge of the classic pathological features of inflammatory neuropathies, attempts at molecular classification and genetic determinants, the utilization of in vitro and in vivo animal models to determine pathogenic mechanisms at the interface between the systemic circulation and the peripheral nervous system relevant to these disorders and prospects for future potential molecular pathology biomarkers and targets for specific therapeutic intervention.

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Class II antigen expression in peripheral neuropathies

Cited by 41 publications

References 24 publications

Expression of antigen processing and presenting molecules by Schwann cells in inflammatory neuropathies

Expression of antigen processing and presenting molecules by Schwann cells in inflammatory neuropathies

β4 integrin and other Schwann cell markers in axonal neuropathy

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

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