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Humoral and cellular immune responses to myelin protein peptides in Chronic Inflammatory Demyelinating Polyradiculoneuropathy
  1. Lara Sanvito (lara.sanvito{at}nottingham.ac.uk)
  1. University of Nottingham, Division of Clinical Neurology, United Kingdom
    1. Anna Makowska (popywhite60{at}hotmail.com)
    1. King's College London, United Kingdom
      1. Mohamed Mahdi-Rogers (mohamed.mahdi-rogers{at}kcl.ac.uk)
      1. King's College London, United Kingdom
        1. Robert DM Hadden (robert.hadden{at}nhs.net)
        1. King's College London, United Kingdom
          1. Mark Peakman (mark.peakman{at}kcl.ac.uk)
          1. King's College London, United Kingdom
            1. Norman Gregson (ngregson{at}ion.ucl.ac.uk)
            1. King's College London, United Kingdom
              1. Raffaello Nemni (raffaello.nemni{at}unimi.it)
              1. Don C. Gnocchi Foundation, Italy
                1. Richard AC Hughes (richard.a.hughes{at}kcl.ac.uk)
                1. Department of Clinical Neurosciences, United Kingdom

                  Abstract

                  Objectives: We sought evidence that chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an autoimmune disease by studying cellular and humoral immune responses to peripheral nerve myelin proteins.

                  Methods: We studied 40 CIDP, 36 healthy control subjects (HC) and subjects with non-immune mediated neuropathies (other neuropathies, ON) for antibodies by ELISA and cellular responses by cytokine ELISPOT (INF-γ, IL-10) and ELISA (IL-17) to synthetic peptides representing P0, P2 and PMP22.

                  Results: Antibodies to P0, P2 or PMP22 peptides were detected in only a minority of CIDP, both not treated (nT-CIDP) and treated (T-CIDP). IgG antibodies to P280-105 were significantly more frequent in CIDP than in HC (4/30 versus 0/32; p<0.05) but the difference from ON (1/25) was not significant. In ELISPOT assays, IFNγ was detected at low frequency in CIDP and did not differ from HC or ON. In contrast, IL-10 responses against P21-85 were more frequent in nT and T-CIDP (7/24 and 3/16) than HC (0/36; p<0.001 and p<0.05, respectively). The production of IL-17 in cell culture supernatants was not increased.

                  Conclusions: Antibodies to non-conformational antigenic epitopes of myelin proteins rarely occur in CIDP. None of the myelin protein peptides elicited IFN-γ responses but P2 elicited IL-10 responses significantly more often in CIDP patients than in controls. This reactivity may be part of an antigen specific Th2 type pathogenetic or regulatory mechanism or represent a transitory epiphenomenon due to nerve damage. In our study P2 was the protein antigen most likely to be involved in the aberrant immune responses in CIDP.

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