Autoimmunoreactivity to Schwann cells in patients with inflammatory neuropathies
Inflammatory demyelinating neuropathies are characterized by a loss of peripheral nerve myelin. Myelin breakdown is thought to result from an autoimmune reaction towards nerve components. Schwann cells play a crucial role in the synthesis and maintenance of peripheral nerve myelin. An immune attack...
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| Veröffentlicht in: | Brain (London, England : 1878) England : 1878), 2003-02, Vol.126 (2), p.361-375 |
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| creator | Kwa, Marcel S. G. van Schaik, Ivo N. De Jonge, Rosalein R. Brand, Anneke Kalaydjieva, Luba van Belzen, Nico Vermeulen, Marinus Baas, Frank |
| description | Inflammatory demyelinating neuropathies are characterized by a loss of peripheral nerve myelin. Myelin breakdown is thought to result from an autoimmune reaction towards nerve components. Schwann cells play a crucial role in the synthesis and maintenance of peripheral nerve myelin. An immune attack targeting Schwann cells could therefore affect myelin integrity, leading to disease. We studied the reactivity of sera from patients with Guillain–Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) towards Schwann cells using immunofluorescence microscopy. We found 24% of the GBS (56 out of 233) and 26% of the CIDP (12 out of 46) patients to have circulating immunoglobulin G autoantibodies against proliferating, non‐myelinating human Schwann cells. In contrast, healthy donors showed positive staining in only two out of 34 sera. No reaction was found with sera from patients with non‐inflammatory neurological disorders. Immunofluorescence was localized at the distal tips (leading lamella) of the Schwann cell processes. Distal tips of neurites (nerve‐growth‐cones) of in vitro differentiated non‐myelinated hNT2 neurons also stained strongly. GBS and CIDP serum immunoreactivity was also observed in teased nerve fibre preparations. These data suggest that, at least part of the immunoreactivity is not directed against myelin, but towards non‐myelin proteins and epitopes possibly involved in Schwann cell–axon interaction. |
| doi_str_mv | 10.1093/brain/awg030 |
| format | Article |
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G. ; van Schaik, Ivo N. ; De Jonge, Rosalein R. ; Brand, Anneke ; Kalaydjieva, Luba ; van Belzen, Nico ; Vermeulen, Marinus ; Baas, Frank</creator><creatorcontrib>Kwa, Marcel S. G. ; van Schaik, Ivo N. ; De Jonge, Rosalein R. ; Brand, Anneke ; Kalaydjieva, Luba ; van Belzen, Nico ; Vermeulen, Marinus ; Baas, Frank</creatorcontrib><description>Inflammatory demyelinating neuropathies are characterized by a loss of peripheral nerve myelin. Myelin breakdown is thought to result from an autoimmune reaction towards nerve components. Schwann cells play a crucial role in the synthesis and maintenance of peripheral nerve myelin. An immune attack targeting Schwann cells could therefore affect myelin integrity, leading to disease. We studied the reactivity of sera from patients with Guillain–Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) towards Schwann cells using immunofluorescence microscopy. We found 24% of the GBS (56 out of 233) and 26% of the CIDP (12 out of 46) patients to have circulating immunoglobulin G autoantibodies against proliferating, non‐myelinating human Schwann cells. In contrast, healthy donors showed positive staining in only two out of 34 sera. No reaction was found with sera from patients with non‐inflammatory neurological disorders. Immunofluorescence was localized at the distal tips (leading lamella) of the Schwann cell processes. Distal tips of neurites (nerve‐growth‐cones) of in vitro differentiated non‐myelinated hNT2 neurons also stained strongly. GBS and CIDP serum immunoreactivity was also observed in teased nerve fibre preparations. These data suggest that, at least part of the immunoreactivity is not directed against myelin, but towards non‐myelin proteins and epitopes possibly involved in Schwann cell–axon interaction.</description><identifier>ISSN: 0006-8950</identifier><identifier>ISSN: 1460-2156</identifier><identifier>EISSN: 1460-2156</identifier><identifier>DOI: 10.1093/brain/awg030</identifier><identifier>PMID: 12538403</identifier><identifier>CODEN: BRAIAK</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Autoantibodies - blood ; autoantibody ; Autoimmunity ; Biological and medical sciences ; Cell Culture Techniques - methods ; Child ; CIDP = chronic inflammatory demyelinating polyneuropathy ; Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction ; Epitopes - immunology ; Female ; GBS = Guillain–Barré syndrome ; GFAP = glial fibrillary acidic protein ; Guillain-Barre Syndrome - immunology ; Guillain–Barré ; HMSN = hereditary sensory and motor neuropathy ; Humans ; IF = immunofluorescence ; IgG = immunoglobulin G ; Immune Sera - immunology ; Immunoglobulin G - blood ; IVIg = intravenous immunoglobulins ; MAb = monoclonal antibody ; Male ; Medical sciences ; Microscopy, Fluorescence ; Middle Aged ; Myelin Sheath - immunology ; NDRG = N‐myc downstream‐regulated gene ; nerve ; Nerve Fibers - immunology ; Nerve Tissue Proteins - immunology ; Nervous system (semeiology, syndromes) ; Neurology ; neuropathy ; PAb = polyclonal antibody ; PBS = phosphate‐buffered saline ; PFA = paraformaldehyde ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - immunology ; Schwann ; Schwann Cells - immunology ; SMA = smooth muscle actin ; Tropical medicine</subject><ispartof>Brain (London, England : 1878), 2003-02, Vol.126 (2), p.361-375</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Feb 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-a5ffd9bc9902da1d32616937ae46958d696c8b1c02bb6273b33fd7cd0e4343e23</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14486932$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12538403$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kwa, Marcel S. G.</creatorcontrib><creatorcontrib>van Schaik, Ivo N.</creatorcontrib><creatorcontrib>De Jonge, Rosalein R.</creatorcontrib><creatorcontrib>Brand, Anneke</creatorcontrib><creatorcontrib>Kalaydjieva, Luba</creatorcontrib><creatorcontrib>van Belzen, Nico</creatorcontrib><creatorcontrib>Vermeulen, Marinus</creatorcontrib><creatorcontrib>Baas, Frank</creatorcontrib><title>Autoimmunoreactivity to Schwann cells in patients with inflammatory neuropathies</title><title>Brain (London, England : 1878)</title><addtitle>Brain</addtitle><description>Inflammatory demyelinating neuropathies are characterized by a loss of peripheral nerve myelin. Myelin breakdown is thought to result from an autoimmune reaction towards nerve components. Schwann cells play a crucial role in the synthesis and maintenance of peripheral nerve myelin. An immune attack targeting Schwann cells could therefore affect myelin integrity, leading to disease. We studied the reactivity of sera from patients with Guillain–Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) towards Schwann cells using immunofluorescence microscopy. We found 24% of the GBS (56 out of 233) and 26% of the CIDP (12 out of 46) patients to have circulating immunoglobulin G autoantibodies against proliferating, non‐myelinating human Schwann cells. In contrast, healthy donors showed positive staining in only two out of 34 sera. No reaction was found with sera from patients with non‐inflammatory neurological disorders. Immunofluorescence was localized at the distal tips (leading lamella) of the Schwann cell processes. Distal tips of neurites (nerve‐growth‐cones) of in vitro differentiated non‐myelinated hNT2 neurons also stained strongly. GBS and CIDP serum immunoreactivity was also observed in teased nerve fibre preparations. These data suggest that, at least part of the immunoreactivity is not directed against myelin, but towards non‐myelin proteins and epitopes possibly involved in Schwann cell–axon interaction.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Autoantibodies - blood</subject><subject>autoantibody</subject><subject>Autoimmunity</subject><subject>Biological and medical sciences</subject><subject>Cell Culture Techniques - methods</subject><subject>Child</subject><subject>CIDP = chronic inflammatory demyelinating polyneuropathy</subject><subject>Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</subject><subject>Epitopes - immunology</subject><subject>Female</subject><subject>GBS = Guillain–Barré syndrome</subject><subject>GFAP = glial fibrillary acidic protein</subject><subject>Guillain-Barre Syndrome - immunology</subject><subject>Guillain–Barré</subject><subject>HMSN = hereditary sensory and motor neuropathy</subject><subject>Humans</subject><subject>IF = immunofluorescence</subject><subject>IgG = immunoglobulin G</subject><subject>Immune Sera - immunology</subject><subject>Immunoglobulin G - blood</subject><subject>IVIg = intravenous immunoglobulins</subject><subject>MAb = monoclonal antibody</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microscopy, Fluorescence</subject><subject>Middle Aged</subject><subject>Myelin Sheath - immunology</subject><subject>NDRG = N‐myc downstream‐regulated gene</subject><subject>nerve</subject><subject>Nerve Fibers - immunology</subject><subject>Nerve Tissue Proteins - immunology</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>neuropathy</subject><subject>PAb = polyclonal antibody</subject><subject>PBS = phosphate‐buffered saline</subject><subject>PFA = paraformaldehyde</subject><subject>Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - immunology</subject><subject>Schwann</subject><subject>Schwann Cells - immunology</subject><subject>SMA = smooth muscle actin</subject><subject>Tropical medicine</subject><issn>0006-8950</issn><issn>1460-2156</issn><issn>1460-2156</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0U2LFDEQBuAgijuu3jxLI-jJdiupJN05LuvHuiwoqCBeQjqddrJ2J2OSdpx_b48zuODFUyD1UFTVS8hjCi8pKDzrkvHhzGy_AcIdsqJcQs2okHfJCgBk3SoBJ-RBzjcAlCOT98kJZQJbDrgiH87nEv00zSEmZ2zxP33ZVSVWH-16a0KorBvHXPlQbUzxLpRcbX1ZLx_DaKbJlJh2VXBzikt97V1-SO4NZszu0fE9JZ_fvP50cVlfv3_77uL8uracYqmNGIZedVYpYL2h_TIXlQob47hUou2lkrbtqAXWdZI12CEOfWN7cBw5Ooan5Pmh7ybFH7PLRU8-74c1wcU564appgXF_wsZCIEg1AKf_gNv4pzCsoSmSnDWcqQLenFANsWckxv0JvnJpJ2moPd56D956EMeC39y7Dl3k-tv8TGABTw7ApOtGYdkgvX51nHeLmfZr1sfnM_F_fpbN-m7lg02Ql9--ar5q5bilWj0Ff4GMPCj7A</recordid><startdate>20030201</startdate><enddate>20030201</enddate><creator>Kwa, Marcel S. G.</creator><creator>van Schaik, Ivo N.</creator><creator>De Jonge, Rosalein R.</creator><creator>Brand, Anneke</creator><creator>Kalaydjieva, Luba</creator><creator>van Belzen, Nico</creator><creator>Vermeulen, Marinus</creator><creator>Baas, Frank</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20030201</creationdate><title>Autoimmunoreactivity to Schwann cells in patients with inflammatory neuropathies</title><author>Kwa, Marcel S. G. ; van Schaik, Ivo N. ; De Jonge, Rosalein R. ; Brand, Anneke ; Kalaydjieva, Luba ; van Belzen, Nico ; Vermeulen, Marinus ; Baas, Frank</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-a5ffd9bc9902da1d32616937ae46958d696c8b1c02bb6273b33fd7cd0e4343e23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Autoantibodies - blood</topic><topic>autoantibody</topic><topic>Autoimmunity</topic><topic>Biological and medical sciences</topic><topic>Cell Culture Techniques - methods</topic><topic>Child</topic><topic>CIDP = chronic inflammatory demyelinating polyneuropathy</topic><topic>Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</topic><topic>Epitopes - immunology</topic><topic>Female</topic><topic>GBS = Guillain–Barré syndrome</topic><topic>GFAP = glial fibrillary acidic protein</topic><topic>Guillain-Barre Syndrome - immunology</topic><topic>Guillain–Barré</topic><topic>HMSN = hereditary sensory and motor neuropathy</topic><topic>Humans</topic><topic>IF = immunofluorescence</topic><topic>IgG = immunoglobulin G</topic><topic>Immune Sera - immunology</topic><topic>Immunoglobulin G - blood</topic><topic>IVIg = intravenous immunoglobulins</topic><topic>MAb = monoclonal antibody</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microscopy, Fluorescence</topic><topic>Middle Aged</topic><topic>Myelin Sheath - immunology</topic><topic>NDRG = N‐myc downstream‐regulated gene</topic><topic>nerve</topic><topic>Nerve Fibers - immunology</topic><topic>Nerve Tissue Proteins - immunology</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>neuropathy</topic><topic>PAb = polyclonal antibody</topic><topic>PBS = phosphate‐buffered saline</topic><topic>PFA = paraformaldehyde</topic><topic>Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - immunology</topic><topic>Schwann</topic><topic>Schwann Cells - immunology</topic><topic>SMA = smooth muscle actin</topic><topic>Tropical medicine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kwa, Marcel S. G.</creatorcontrib><creatorcontrib>van Schaik, Ivo N.</creatorcontrib><creatorcontrib>De Jonge, Rosalein R.</creatorcontrib><creatorcontrib>Brand, Anneke</creatorcontrib><creatorcontrib>Kalaydjieva, Luba</creatorcontrib><creatorcontrib>van Belzen, Nico</creatorcontrib><creatorcontrib>Vermeulen, Marinus</creatorcontrib><creatorcontrib>Baas, Frank</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain (London, England : 1878)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kwa, Marcel S. G.</au><au>van Schaik, Ivo N.</au><au>De Jonge, Rosalein R.</au><au>Brand, Anneke</au><au>Kalaydjieva, Luba</au><au>van Belzen, Nico</au><au>Vermeulen, Marinus</au><au>Baas, Frank</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autoimmunoreactivity to Schwann cells in patients with inflammatory neuropathies</atitle><jtitle>Brain (London, England : 1878)</jtitle><addtitle>Brain</addtitle><date>2003-02-01</date><risdate>2003</risdate><volume>126</volume><issue>2</issue><spage>361</spage><epage>375</epage><pages>361-375</pages><issn>0006-8950</issn><issn>1460-2156</issn><eissn>1460-2156</eissn><coden>BRAIAK</coden><abstract>Inflammatory demyelinating neuropathies are characterized by a loss of peripheral nerve myelin. Myelin breakdown is thought to result from an autoimmune reaction towards nerve components. Schwann cells play a crucial role in the synthesis and maintenance of peripheral nerve myelin. An immune attack targeting Schwann cells could therefore affect myelin integrity, leading to disease. We studied the reactivity of sera from patients with Guillain–Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) towards Schwann cells using immunofluorescence microscopy. We found 24% of the GBS (56 out of 233) and 26% of the CIDP (12 out of 46) patients to have circulating immunoglobulin G autoantibodies against proliferating, non‐myelinating human Schwann cells. In contrast, healthy donors showed positive staining in only two out of 34 sera. No reaction was found with sera from patients with non‐inflammatory neurological disorders. Immunofluorescence was localized at the distal tips (leading lamella) of the Schwann cell processes. Distal tips of neurites (nerve‐growth‐cones) of in vitro differentiated non‐myelinated hNT2 neurons also stained strongly. GBS and CIDP serum immunoreactivity was also observed in teased nerve fibre preparations. These data suggest that, at least part of the immunoreactivity is not directed against myelin, but towards non‐myelin proteins and epitopes possibly involved in Schwann cell–axon interaction.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>12538403</pmid><doi>10.1093/brain/awg030</doi><tpages>15</tpages></addata></record> |
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| subjects | Adolescent Adult Aged Aged, 80 and over Autoantibodies - blood autoantibody Autoimmunity Biological and medical sciences Cell Culture Techniques - methods Child CIDP = chronic inflammatory demyelinating polyneuropathy Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction Epitopes - immunology Female GBS = Guillain–Barré syndrome GFAP = glial fibrillary acidic protein Guillain-Barre Syndrome - immunology Guillain–Barré HMSN = hereditary sensory and motor neuropathy Humans IF = immunofluorescence IgG = immunoglobulin G Immune Sera - immunology Immunoglobulin G - blood IVIg = intravenous immunoglobulins MAb = monoclonal antibody Male Medical sciences Microscopy, Fluorescence Middle Aged Myelin Sheath - immunology NDRG = N‐myc downstream‐regulated gene nerve Nerve Fibers - immunology Nerve Tissue Proteins - immunology Nervous system (semeiology, syndromes) Neurology neuropathy PAb = polyclonal antibody PBS = phosphate‐buffered saline PFA = paraformaldehyde Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - immunology Schwann Schwann Cells - immunology SMA = smooth muscle actin Tropical medicine |
| title | Autoimmunoreactivity to Schwann cells in patients with inflammatory neuropathies |
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