TNF alpha, IFN gamma and IL-2 mRNA expression in CIDP sural nerve biopsies

J Neurol Sci. 1999 Feb 1;163(1):47-52. doi: 10.1016/s0022-510x(99)00009-x.


Proinflammatory cytokines contribute to the regulation of the disease process in inflammatory neuropathies. Cellular localisation of cytokine expression in CIDP nerve biopsies should provide further insight into the pathogenic mechanisms of the disease and the individual cells involved. In this study in situ hybridisation was used to determine the exact localisation and identity of cells that express TNF alpha, IFN gamma and IL-2 mRNA within the CIDP nerve. Paraffin embedded and frozen sural nerve biopsies from three acute phase CIDP patients were used for the study. Sections of these samples were probed with digoxigenin labelled oligoprobes for TNF alpha, IFN gamma and IL-2. The results demonstrate localisation of cytokine expression to the inner rim of the perineurium, epineurial and endoneurial blood vessels and infiltrating inflammatory cells. In addition strong staining for TNF alpha. mRNA was widespread in the endoneurium in areas consistent with/suggestive of Schwann cells. Expression of cytokines in the perineurium and endoneurial blood vessels may have pertinent implications with respect to the breakdown of the blood nerve barrier associated with CIDP. In the very least the potential for an immunomodulatory role may be ascribed to these cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Autoimmune Diseases / immunology*
  • Autoimmune Diseases / pathology
  • Biopsy
  • Chronic Disease
  • Demyelinating Diseases / immunology*
  • Demyelinating Diseases / pathology
  • Histocompatibility Antigens Class II / analysis
  • Humans
  • In Situ Hybridization
  • Inflammation
  • Interferon-gamma / genetics*
  • Interleukin-2 / genetics*
  • Peripheral Nervous System Diseases / immunology*
  • Peripheral Nervous System Diseases / pathology
  • RNA, Messenger / genetics
  • Sural Nerve / immunology*
  • Sural Nerve / pathology
  • Transcription, Genetic*
  • Tumor Necrosis Factor-alpha / genetics*


  • Histocompatibility Antigens Class II
  • Interleukin-2
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma