Thesis

The expression of IL-22 during the development of experimental autoimmune encephalomyelitis (EAE)

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Awarding institution
  • University of Strathclyde
Date of award
  • 2014
Thesis identifier
  • T13738
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Abstract
  • Interleukin (IL)-22 (IL-22) is a member of the IL-10 family, which is an important regulator of the inflammatory response. IL-22 is produced by Th17 cells, which play a key immunopathogenic role in many immune disorders. However, the exact function of IL-22 in the development of central nervous system (CNS) inflammatory diseases such as multiple sclerosis (MS) remains unclear. This study aims to understand better the role of IL-22 in the development of MS disease by examining its expression levels in the peripheral immune organs and CNS spinal cord (SC) tissues of experimental autoimmune encephalomyelitis (EAE) mice and investigates whether the expression levels of IL-22 correlate with the CNS inflammation. EAE was induced by immunizing C57BL/6 female mice with MOG35-55 peptide emulsified in Complete Freunds Adjuvant (CFA) subcutaneously, together with intraperitoneal injection of pertussis toxin (PTX). EAE clinical score was recorded daily and spleen and SC tissues were harvested at days 9, 17 and 28 post-immunization to assess cytokine secretion profile and tissue pathology. Our data demonstrate that MOG35-55 immunized mice start to develop EAE around day 9 and reached peak at day 15 while PBS-CFA immunized mice remained unaffected. ELISA data of the spleen cell cultures show that cells from MOG-CFA immunized mice produced higher levels of antigen-specific IL-22, IL-17A and IFN-γ at day 9 and day 17 when compared with PBS immunized mice. Furthermore, immunohistological staining data show that whilst naïve/PBS-CFA SC tissues expressed IL-22, the expression level was significantly increased in the SC of MOG-CFA mice at day 9 and 17. Furthermore, IL-22 was generally detected in both white and grey matter within the SC and was highly expressed by astrocytes (and not axons or neurons) in EAE at the peak of inflammation. Our data therefore suggest that IL-22 may play a pathogenic role in the neurological autoimmune diseases, possibly through divergent roles in both the peripheral immune and CNS systems.
Resource Type
DOI
Date Created
  • 2014
Former identifier
  • 1032596

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