title: Humoral and cellular immune responses to myelin protein peptides in chronic inflammatory demyelinating polyradiculoneuropathy.
abstract: OBJECTIVE
  Evidence that chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an autoimmune disease was sought, by studying cellular and humoral immune responses to peripheral nerve myelin proteins.
  
  
  METHODS
  40 CIDP, 36 healthy control subjects (HC) and subjects with non-immune mediated neuropathies (other neuropathies, ON) for antibodies were studied by ELISA and cellular responses by cytokine ELISPOT (INF gamma, IL10) and ELISA (IL17) 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 P2(80-105) were significantly more frequent in CIDP than in HC (4/30 vs 0/32; p<0.05) but the difference from ON (1/25) was not significant. In ELISPOT assays, IFN gamma was detected at a low frequency in CIDP and did not differ from HC or ON. In contrast, IL10 responses against P2(1-85) 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 IL17 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 gamma responses, but P2 elicited IL10 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.
authors.affiliation: Department of Clinical Neuroscience, King's College London, Guy's Hospital, London, UK. lara.sanvito@nottingham.ac.uk
authors.forename: L
authors.initials: L
authors.lastname: Sanvito
authors.forename: A
authors.initials: A
authors.lastname: Makowska
authors.forename: M
authors.initials: M
authors.lastname: Mahdi-Rogers
authors.forename: R D M
authors.initials: RD
authors.lastname: Hadden
authors.forename: M
authors.initials: M
authors.lastname: Peakman
authors.forename: N
authors.initials: N
authors.lastname: Gregson
authors.forename: R
authors.initials: R
authors.lastname: Nemni
authors.forename: R A C
authors.initials: RA
authors.lastname: Hughes
mesh_terms: D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000097:blood*; D002478:Cells, Cultured / Q000276:immunology; D016207:Cytokines / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology*; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D007371:Interferon-gamma / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D020381:Interleukin-17 / Q000097:blood; D008297:Male; D008875:Middle Aged; D018993:Myelin P0 Protein / Q000276:immunology*; D009185:Myelin Proteins / Q000276:immunology*; D010446:Peptide Fragments / Q000276:immunology*; D020277:Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D016207:Cytokines; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D020381:Interleukin-17; D018993:Myelin P0 Protein; D009185:Myelin Proteins; C425263:P2 peptide; C073687:PMP22 protein, human; D010446:Peptide Fragments; D016753:Interleukin-10; D007371:Interferon-gamma