The Role of HTLV-1 Related Endogenous Retroviral Sequence in the Etiopathogenesis Of Systemic Lupus Erythematosus

Persistent Link:
http://hdl.handle.net/10150/312499
Title:
The Role of HTLV-1 Related Endogenous Retroviral Sequence in the Etiopathogenesis Of Systemic Lupus Erythematosus
Author:
Leo, Nancy Stefany
Issue Date:
2013
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease. HTLV-1 Related Endogenous Sequence (HRES-1), a human endogenous retrovirus, produces 2 retroviral-like Gag capsid proteins (p8 and p15) that share significant sequence homology to the U1-subunit of the small ribonucleoprotein complex (U1sn-RNP), an autoantigen of lupus. The central hypothesis is that molecular mimicry between HRES-1 and U1sn-RNP serves as a priming event in SLE via the production of cross-reactive autoantibodies. Anti-HRES-1/U1sn-RNP serological responses in subjects with SLE and comparison populations were characterized. An overlapping peptide set mapping the HRES-1 p8 and p15 proteins was used. SLE subjects produce IgG to several regions of HRES-1. Healthy subjects or those with RA, HIV-1 infection, or HTLV-1-infection produced no significant anti-HRES-1 IgG. Anti-HRES-1 antibodies deposited in the kidneys of patients with SLE glomerulonephritis were identified. Our data suggests that HRES-1 plays a role in SLE by means of a molecular mimicry mechanism with U1sn-RNP.
Type:
text; Electronic Thesis
Keywords:
immune complexes; molecular mimicry; overlapping peptide set; systemic lupus erythematosus; U1sn-RNP; Molecular & Cellular Biology; HRES-1
Degree Name:
M.S.
Degree Level:
masters
Degree Program:
Graduate College; Molecular & Cellular Biology
Degree Grantor:
University of Arizona
Advisor:
Adelman, Miranda K.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen
dc.titleThe Role of HTLV-1 Related Endogenous Retroviral Sequence in the Etiopathogenesis Of Systemic Lupus Erythematosusen_US
dc.creatorLeo, Nancy Stefanyen_US
dc.contributor.authorLeo, Nancy Stefanyen_US
dc.date.issued2013-
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractSystemic Lupus Erythematosus (SLE) is a complex autoimmune disease. HTLV-1 Related Endogenous Sequence (HRES-1), a human endogenous retrovirus, produces 2 retroviral-like Gag capsid proteins (p8 and p15) that share significant sequence homology to the U1-subunit of the small ribonucleoprotein complex (U1sn-RNP), an autoantigen of lupus. The central hypothesis is that molecular mimicry between HRES-1 and U1sn-RNP serves as a priming event in SLE via the production of cross-reactive autoantibodies. Anti-HRES-1/U1sn-RNP serological responses in subjects with SLE and comparison populations were characterized. An overlapping peptide set mapping the HRES-1 p8 and p15 proteins was used. SLE subjects produce IgG to several regions of HRES-1. Healthy subjects or those with RA, HIV-1 infection, or HTLV-1-infection produced no significant anti-HRES-1 IgG. Anti-HRES-1 antibodies deposited in the kidneys of patients with SLE glomerulonephritis were identified. Our data suggests that HRES-1 plays a role in SLE by means of a molecular mimicry mechanism with U1sn-RNP.en_US
dc.typetexten
dc.typeElectronic Thesisen
dc.subjectimmune complexesen_US
dc.subjectmolecular mimicryen_US
dc.subjectoverlapping peptide seten_US
dc.subjectsystemic lupus erythematosusen_US
dc.subjectU1sn-RNPen_US
dc.subjectMolecular & Cellular Biologyen_US
dc.subjectHRES-1en_US
thesis.degree.nameM.S.en_US
thesis.degree.levelmastersen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineMolecular & Cellular Biologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorAdelman, Miranda K.en_US
dc.contributor.committeememberAdelman, Miranda K.en_US
dc.contributor.committeememberBurd, Gail D.en_US
dc.contributor.committeememberAhmad, Nafeesen_US
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