ACR Meeting Abstracts

ACR Meeting Abstracts

  • Meetings
    • ACR Convergence 2024
    • ACR Convergence 2023
    • 2023 ACR/ARP PRSYM
    • ACR Convergence 2022
    • ACR Convergence 2021
    • ACR Convergence 2020
    • 2020 ACR/ARP PRSYM
    • 2019 ACR/ARP Annual Meeting
    • 2018-2009 Meetings
    • Download Abstracts
  • Keyword Index
  • Advanced Search
  • Your Favorites
    • Favorites
    • Login
    • View and print all favorites
    • Clear all your favorites
  • ACR Meetings

Abstract Number: 646

Expression Of Interferon-Inducible Gene (Lymphocyte Antigen 6 Complex Locus E) In Systemic Lupus Erythematosus Patients and Its Association With Disease Activity

Eman Omran1, Tayseer M Khidre2, Eman Alkady3, Eman Mosaad4 and Mona Hussein Abd Elsamea3, 1Rheumatology and Clincal Immunology, Assiut University- Faulty of Medicne, Assiut, Egypt, 2Assiut University, Faculty of Medicine, Assiut, Egypt, 3Assiut University- Faculty of Medicine, Assiut, Egypt, 4AssiutUniversity- Faculty of Medicine, Assiut, Egypt

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: complement and interferons, SLE

  • Tweet
  • Email
  • Print
Session Information

Title: Systemic Lupus Erythematosus - Human Etiology and Pathogenesis: Mechanisms and Biomarkers

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by immune dysregulation resulting in the production of antinuclear and other autoantibodies, generation of circulating immune complexes, and activation of the complement system. The disease course of SLE is heterogeneous, affecting different individuals with a wide range of manifestations.

      Recent genetic studies identified a group of type I Interferon-inducible genes (IFIGs) that are significantly upregulated in peripheral blood cells from SLE patients. IFIGs show expression of  5 types  [Myxovirus resistance 1 (Mx1), Oligoadenylate synthetase (OAS)1, and Lymphocyte antigen 6 complex, locus E (Ly6e), Oligoadenylate synthetase–like (OASL), and Interferon-inducible protein (clone IFI-15K) (ISG15)]  in peripheral blood sample from  SLE patients.

The aim of the study was to assess the expression of type I IFIGs (LY6E) in patients with SLE. In addition, we evaluated the association of its levels with disease activity and/or severity, and laboratory markers.

Methods:

Peripheral blood sample were obtained from 40 SLE patients and 25 healthy donors and total RNA was extracted and reverse transcribed into complementary DNA. Level of expression of type I IFIGs (LY6E) was measured by real time polymerase chain reaction (PCR-RT), after which comparisons were performed between SLE patients and control individuals.

   Disease status was assessed according to the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index.

Results:

     Type I IFIGs (LY6E) was highly expressed in SLE patients compared with normal controls (P<0.000). Type I IFIGs (LY6E) was positively associated with the SLEDAI score (p<0.02). Elevated type I IFIGs (LY6E) was also associated with the presence of cumulative organ damage SLICC/ACR-Damage Index (P<0.01).

    Type I IFIGs (LY6E) was positively correlated with anti–double-stranded DNA (anti-dsDNA) antibodies (P<0.01) and negatively correlated with C3 (P<0.03). LY6E expression levels was positively associated with proteinuria (P <0.009).

Conclusion:

Type I IFIGs (LY6E) was highly expressed in SLE patients, and higher expression of LY6E gene in SLE patients is closely correlated with disease activity, degree of organ damage, proteinuria, anti-dsDNA antibody and hypocomplementemia. Besides, its elevated level may predict SLE flares. 

The data suggest that type I IFIGs (LY6E) may contribute to SLE pathogenesis and the finding of this study will shed new light on dysregulation of the immune system and the involvement of inflammation in the initiation and perpetuation of autoimmunity.


Disclosure:

E. Omran,
None;

T. M Khidre,
None;

E. Alkady,
None;

E. Mosaad,
None;

M. Hussein Abd Elsamea,
None.

  • Tweet
  • Email
  • Print

« Back to 2013 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/expression-of-interferon-inducible-gene-lymphocyte-antigen-6-complex-locus-e-in-systemic-lupus-erythematosus-patients-and-its-association-with-disease-activity/

Advanced Search

Your Favorites

You can save and print a list of your favorite abstracts during your browser session by clicking the “Favorite” button at the bottom of any abstract. View your favorites »

All abstracts accepted to ACR Convergence are under media embargo once the ACR has notified presenters of their abstract’s acceptance. They may be presented at other meetings or published as manuscripts after this time but should not be discussed in non-scholarly venues or outlets. The following embargo policies are strictly enforced by the ACR.

Accepted abstracts are made available to the public online in advance of the meeting and are published in a special online supplement of our scientific journal, Arthritis & Rheumatology. Information contained in those abstracts may not be released until the abstracts appear online. In an exception to the media embargo, academic institutions, private organizations, and companies with products whose value may be influenced by information contained in an abstract may issue a press release to coincide with the availability of an ACR abstract on the ACR website. However, the ACR continues to require that information that goes beyond that contained in the abstract (e.g., discussion of the abstract done as part of editorial news coverage) is under media embargo until 10:00 AM ET on November 14, 2024. Journalists with access to embargoed information cannot release articles or editorial news coverage before this time. Editorial news coverage is considered original articles/videos developed by employed journalists to report facts, commentary, and subject matter expert quotes in a narrative form using a variety of sources (e.g., research, announcements, press releases, events, etc.).

Violation of this policy may result in the abstract being withdrawn from the meeting and other measures deemed appropriate. Authors are responsible for notifying colleagues, institutions, communications firms, and all other stakeholders related to the development or promotion of the abstract about this policy. If you have questions about the ACR abstract embargo policy, please contact ACR abstracts staff at [email protected].

Wiley

  • Online Journal
  • Privacy Policy
  • Permissions Policies
  • Cookie Preferences

© Copyright 2025 American College of Rheumatology