dc.contributor.author |
Jammaz, Rana Fadllala, |
dc.date.accessioned |
2017-08-30T14:27:34Z |
dc.date.available |
2017-08-30T14:27:34Z |
dc.date.issued |
2016 |
dc.date.submitted |
2016 |
dc.identifier.other |
b18933233 |
dc.identifier.uri |
http://hdl.handle.net/10938/11058 |
dc.description |
Thesis. M.Sc. American University of Beirut. Department of Experimental Pathology, Microbiology and Immunology 2016. W 4 J327r 2016 |
dc.description |
Advisor: Dr. Elias Rahal, Ph.D., Assistant Professor; Department of Experimental Pathology, Immunology and Microbiology Committee members: Dr. Alexander Abdelnoor, Ph.D., Professor and Chairperson; Department of Experimental Pathology, Immunology and Microbiology ; Dr. Ghassan Matar, Ph.D., Professor, Department of Experimental Pathology, Immunology and Microbiology ; Margret Shirinian, Ph.D., Instructor, Department of Experimental Pathology, Immunology and Microbiology. |
dc.description |
Includes bibliographical references (leaves 31-35) |
dc.description.abstract |
Background: The Epstein-Barr virus (EBV) is a DNA virus that establishes latent infections that often reactivats. Previous studies demonstrated a relation between EBV and autoimmune diseases such as rheumatoid arthritis, multiple sclerosis and systemic lupus erythematosus. A previous study conducted at the Department of Experimental Pathology, Immunology and Microbiology demonstrated a relation between injecting EBV DNA and increased production of IL-17 in mice. IL-17 is a proinflammatory cytokine associated with various autoimmune diseases. On the other hand, reports investigating interaction of EBV with Toll-like receptors (TLRs) showed that EBV DNA is possibly recognized by TLR9.Therefore, the study at hand focused on the role of TLR9 on the enhancement of IL-17 production caused by EBV DNA in BALB-c mouse peripheral blood mononuclear cells (PBMCs) in culture as well as in BALB-c mice in vivo. Methods (Ex vivo): Blood was collected from 11 BALB-c mice and PBMCs were separated using Ficoll-isopaque. Mouse PBMCs were then cultured for 24 hours with EBV DNA, EBV DNA and the TLR9 inhibitor ODN 2088, TLR9 inhibitor alone or with Staphyloccocus epidermidis DNA used as a non-viral DNA control. Untreated cells were included as well. Subsequently, the level of IL-17 was assessed in culture supernatants with an enzyme-linked immunosorbent assay (ELISA). Methods (In vivo): To assess the role of TLR9 in the enhancement of IL-17 caused by EBV DNA in vivo, 45 female BALB-c mice were used. Mice were divided into 5 groups each containing 9 mice. Mouse groups were injected with EBV DNA, EBV DNA and the TLR9 inhibitor, TLR9 inhibitor alone or with S. epidermidis DNA. A group that was injected with sterile distilled water was assessed as well. Three mice were sacrificed per group on days 3, 6, and 9 post-injection. Blood was collected by cardiac puncture and pooled per group per time point. Serum was then collected to assess IL-17 levels by ELISA. Results: Mouse PBMCs treated with EBV DNA displayed increased levels of IL-17; |
dc.format.extent |
1 online resource (35 leaves) |
dc.language.iso |
eng |
dc.relation.ispartof |
Theses, Dissertations, and Projects |
dc.subject.classification |
W 4 J327r 2016 |
dc.subject.lcsh |
Dissertations, Academic. |
dc.subject.lcsh |
Autoimmunity. |
dc.subject.lcsh |
Epstein-Barr virus. |
dc.subject.lcsh |
Toll-Like Receptors. |
dc.subject.lcsh |
Interleukin -17. |
dc.title |
Role of Toll-Like Receptor 9 in Epstein-Barr Virus DNA-Triggered IL-17 production in BALB-c mice - |
dc.type |
Thesis |
dc.contributor.department |
Department of Experimental Pathology, Microbiology and Immunology,Faculty of Medicine, |
dc.contributor.institution |
American University of Beirut. |