Increase of pro‐inflammatory cytokines in chronic sensory ataxic neuropathies

  • L Sanvito
  • , G Santuccio
  • , L Speciale
  • , M Sgandurra
  • , L Merlino
  • , L Ceresa
  • , P Ferrante
  • , R Nemni

Research output: Contribution to journalMeeting Abstractpeer-review

Abstract

Chronic sensory ataxic neuropathies (CSAN) are characterised by a predominant involvement of sensory large fibers. We previously demonstrated the presence of serum antibodies against neuropathy‐related antigens in about 50% of these patients. The aim of our study was to analyse peripheral T and B cell subsets and cytokine network in CSAN patients in order to evaluate their immunological profile. We studied 10 CSAN patients. ELISA test detected the presence of neuropathy‐related autoantibodies in 5 out of 10 patients. We evaluated, by flow cytometry, CD3+, CD3 + DRII+, CD4+, CD8+, CD16+ and CD19+ cells subset distribution, and intracellular IL2, INFg, IL1, IL6, IL10 and TNFa production by CD4+, CD8+ and CD14+ cells. Results were compared with healthy controls (HC); statistical analysis was performed. Compared to HC, CSAN patients showed no significant difference in lymphocyte subset distribution. We found a significant increase of IL6 in CD4+, CD8+ and CD14+ cells. INFg and TNFa were increased in CD4+ cells. TNFa was decreased in CD14+. Our results show an increase of pro‐inflammatory cytokines not associated with imbalance of T and B cells subsets. These data support an activation of the immune system in CSAN, as previously suggested by the detection of neuropathy‐related autoantibodies.
Original languageEnglish
Pages (from-to)106
Number of pages1
JournalJournal of the Peripheral Nervous System
Volume9
Issue number2
Early online date22 Apr 2004
DOIs
Publication statusPublished - Jun 2004
Event9th Meeting of the Italian Peripheral NerveStudy Group (Joint Meeting with the Italian Associationof Myology) - Taormina, Italy
Duration: 6 May 20048 May 2004

Fingerprint

Dive into the research topics of 'Increase of pro‐inflammatory cytokines in chronic sensory ataxic neuropathies'. Together they form a unique fingerprint.

Cite this