Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509153
Title: Epstein-Barr Virus (EBV) latent membrane protein 1 (LMP1) peptides as inducers of regulatory cells to treat autoimmune haemolytic anaemia
Author: Zamzami, Omar M.
Awarding Body: University of Aberdeen
Current Institution: University of Aberdeen
Date of Award: 2009
Availability of Full Text:
Access through EThOS:
Full text unavailable from EThOS. Please try the link below.
Access through Institution:
Abstract:
Immune responses to Epstein-Barr Virus (EBV) encoded Latent Membrane Protein 1 (LMP1) peptides in seropositive donors are dominated by the induction of IL-10 secretion. These IL-10 responses, characteristic of T regulatory 1 (Tr1) cells, were able to inhibit T-cell proliferation and interferon-γ (IFN-γ) section induced by other antigens. Furthermore, this inhibition was specific to the co-presented antigen and persisted after LMP1 peptide had been removed. Thus, it may be possible to exploit such specific induction therapeutically to inhibit pathogenic responses in immune-mediated diseases. The current study was initiated to confirm and extend these findings and then to investigate the ability of LMP1 peptides to inhibit pathogenic responses to Rh autoantigen in AIHA patients in vitro. Inhibitory properties of LMP1 peptides were confirmed, although most such inhibition appeared non-specific and was not associated with IL-10. Inhibition appeared to involve an effect on antigen presenting cells. When autologous red cells or RhD peptides were used as stimulating antigens in patients with AIHA, IL-17 responses were more frequent than IFN-γ secretion. Furthermore, disease activity correlated better with IL-17 responses than TH1 responses. These data therefore suggest that the pathogenesis of AIHA has a substantial Th17 component. Finally, these autoreactive responses could be inhibited by LMP1 peptides.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.509153  DOI: Not available
Keywords: Autoimmune diseases ; Epstein-Barr virus
Share: