Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.558160
Title: Effects of virulence and fraction 1 antigens from Yersinia pestis on the human innate immune system
Author: De Seabra Rodrigues Dias, Ivo Ricardo
Awarding Body: University of Sussex
Current Institution: University of Sussex
Date of Award: 2012
Availability of Full Text:
Access through EThOS:
Access through Institution:
Abstract:
Yersinia pestis, the aetiological agent of plague, is responsible for a disease that has killed over 200 million people throughout history and generated three pandemics. This bacterium's terrible success in causing disease is owed greatly to the virulence factors it expresses. Two of these factors are V antigen (LcrV) and F1 antigen (Caf1), both of which are two major antigens which the immune system produces antibodies against. V antigen is already known to have vital roles in Y. pestis gene expression and translocating other virulence factors into the host cells as well as having some immunosuppressive effects while F1 antigen is better known for possessing an antiphagocytic effect. The effects that these two antigens have in modulating the innate immune system of Mono Mac 6 cells were studied, such as modulation of expression of pattern recognition receptors (PRRs), in particular Toll-like receptors (TLRs), activation of NF-κB and secretion of cytokines, particularly those involved in inflammatory responses, as well as localising where in the cell these antigens target to. It was demonstrated that both V and F1 antigens possess immunosuppressive abilities, such as downregulation of TLRs as well as inhibitition of NF-κB activation and suppression of secretion of the cytokines TNF-α, IL-6 and IL-10. Furthermore, stimulation with only either V or F1 antigens can upregulate expression of the scavenger receptor CD36 and are capable of inducing secretion of the anti-inflammatory cytokine IL-10. V and F1 antigens were found to localise in the Golgi apparatus 30 minutes after stimulation and it was also determined that these antigens interfere with the signalling molecule MyD88.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.558160  DOI: Not available
Keywords: QD0415 Biochemistry ; QR0075 Bacteria
Share: