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: 2810

The Presence of HLA-B27 Increases Severity of Arthritis but Does Not Appear to Influence New Bone Formation in Different in Vitro and in Vivo Models

Barbara Neerinckx1, Kerri Heritage2, Jacqueline Shaw3, S. Kollnberger3, Paul Bowness3 and Rik Lories1, 1Rheumatology, UZ Leuven, Leuven, Belgium, 2Laboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Center, KU Leuven and University Hospitals Leuven., Leuven, Belgium, 3Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, United Kingdom

Meeting: 2015 ACR/ARHP Annual Meeting

Date of first publication: September 29, 2015

Keywords: Ankylosing spondylitis (AS)

  • Tweet
  • Click to email a link to a friend (Opens in new window) Email
  • Click to print (Opens in new window) Print
Session Information

Date: Tuesday, November 10, 2015

Title: Spondylarthropathies and Psoriatic Arthritis Pathogenesis, Etiology Poster I

Session Type: ACR Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose: The strong genetic association between the HLA-B27 gene and ankylosing spondylitis (AS) has been known for over 40 years. Among AS patients, HLA-B27 positivity is associated with worse disease outcome. The long-term outcome of AS is determined by both inflammation and structural damage. The latter is characterized by new cartilage and bone formation, often leading to ankylosis. In this study, we investigated the in vitro and in vivo impact of HLA-B27 (over)expression in model systems of cartilage and bone formation. 

Methods:

We used different in vitro systems mimicking endochondral bone formation. We set up micromasses with ATDC5 cells and human periosteal derived cells (hPDCs) transduced with a HLA-B27 or HLA-B7 (as a control) lentiviral vector. Micromasses were kept for 21 (ATDC5) or 14 (hPDCs) days in culture. RNA extraction and colorimetric tests were performed at different time points (d1, d7, d14, d21). For the ATDC5 cells, after 14 days the chondrogenic medium was switched to mineralization medium. To specifically study osteogenesis in hPDCs, cells were kept in monolayer for 28 days and stimulated with osteogenic media. We also set up micromasses from limb bud cells derived from HLA-B27 transgenic and wild-type (WT) C57BL/6 mice embryos at day 12.5E. These cells are also known to undergo endochondral bone formation in vitro. Samples were taken for RNA extraction at d1, d7 and d14. Chondrogenesis (Col II, Aggrecan, Col X) and osteogenesis associated markers (OSC, ALP, Runx2) were studied by quantitative RT-PCR.  Stainings with alcian blue, alizarin red, picosirius red and safranin O were performed to measure proteoglycans, mineralization and collagens. For the in vivostudy, we induced collagen antibody induced arthritis (CAIA) in HLA-B27 transgenic and WT C57BL/6 mice (n=10 in each group). Clinical scoring was performed twice a week. µCT scans were performed at baseline and 3 and 6 weeks after disease induction to study new bone formation. Statistical analyses were performed by 2 way ANOVA taking into account repeated measurements as appropriate.

Results: There was no difference in expression of Col II, Aggrecan or Col X in the HLA-B27 ATDC5 micromasses compared to the HLA-B7 micromasses. There was no difference between the stainings at the different time points. For the hPDC micromasses, there was no difference in expression of the chondrogenesis markers between HLA-B27 and HLA-B7 micromasses. Stainings with alcian blue could not show any difference between the two conditions. Expression of osteogenesis markers en alizarin red staining was comparable in the HLA-B27 and the HLA-B7 hPDCs in monolayer. The limb bud micromasses showed no difference in expression of chondrogenesis associated genes between HLA-B27 transgenic and WT embryos. In the CAIA experiment, the HLA-B27 transgenic mice showed more severe arthritis compared to WT mice. µCT analysis showed no increased bone formation in the post-inflammatory phase when HLA-B27 transgenic mice were compared to WT. 

Conclusion: The presence of HLA-B27 seems to enhance joint inflammation in the CAIA model in C57BL/6 mice. These in vivo and the in vitrodata do not support a direct role for HLA-B27 in new cartilage or bone formation leading to ankylosis.


Disclosure: B. Neerinckx, None; K. Heritage, None; J. Shaw, None; S. Kollnberger, None; P. Bowness, None; R. Lories, None.

To cite this abstract in AMA style:

Neerinckx B, Heritage K, Shaw J, Kollnberger S, Bowness P, Lories R. The Presence of HLA-B27 Increases Severity of Arthritis but Does Not Appear to Influence New Bone Formation in Different in Vitro and in Vivo Models [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/the-presence-of-hla-b27-increases-severity-of-arthritis-but-does-not-appear-to-influence-new-bone-formation-in-different-in-vitro-and-in-vivo-models/. Accessed .
  • Tweet
  • Click to email a link to a friend (Opens in new window) Email
  • Click to print (Opens in new window) Print

« Back to 2015 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/the-presence-of-hla-b27-increases-severity-of-arthritis-but-does-not-appear-to-influence-new-bone-formation-in-different-in-vitro-and-in-vivo-models/

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