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: 2348

Activatory Fc Gamma Receptor IV Plays a Crucial Role in Pathogenesis of Experimental Immune Complex Mediated Chronic Arthritis

Irene Di Ceglie1, Arjen Blom1, Sjef Verbeek2, Peter van der Kraan3, Wim van den Berg1 and Peter L. van Lent1, 1Experimental Rheumatology, Experimental Rheumatology, Radboud University, Nijmegen, Netherlands, 2Human Genetic, Human Genetic, Leiden University Medical Center, Leiden, Netherlands, 3Experimental Rheumatology, Radboud University, Nijmegen, Netherlands

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Fc receptors and rheumatoid arthritis (RA)

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

Title: Rheumatoid Arthritis - Animal Models

Session Type: Abstract Submissions (ACR)

Background/Purpose

Rheumatoid arthritis is characterized by Immune complex dependent chronic joint inflammation and severe cartilage and bone destruction. Earlier we found that in the absence of activatory FcγRI and III, joint destruction during the early murine phase of antigen-induced arthritis (AIA) was protected (1) but the role of FcγRIV has not yet been elucidated.

Methods

AIA was induced by injection of mBSA into the knee joint of FcγRI,II,III -/-, FcγI,II,III,IV-/-and wild type (WT) control mice previously immunized with mBSA/CFA.  Histology of total knee joints was taken at day 7 and 21 after arthritis induction. Joint inflammation was scored using an arbitrary scale. Cartilage damage was measured as proteoglycan (PG) depletion. Bone destruction was determined using an arbitrary score. mBSA antibody titers were determined using ELISA.

Results

Both KO strains showed antibody titers against mBSA comparable to immunized control mice. In the early phase of AIA  (day 7), joint inflammation was significantly higher in FcγRI,II,III-/- (infiltrate 47% and exudate 107% higher) when compared to WT controls. In FcγRI,II,III,IV-/-however, although comparable antibody titers, inflammation was significantly lower (infiltrate 30% and exudate 46% lower) than in WT controls. Early cartilage destruction was protected in both strains reflected by significantly lower PG depletion (34% and 20% lower respectively) when compared to their WT controls.  

During the chronic phase at day 21, joint inflammation in FcγI/II/III-/- was still significantly higher (infiltrate 450% and exudate 170% higher) when compared to WT controls. Protection of cartilage damage seen in early AIA was lost and PG depletion significantly increased in FcγRI,II,III -/-by 260 %. Bone erosion also increased by 150%. These results suggest that FcγRI and III regulate destruction in the early phase whereas FcγRIV may be more important in chronic stages of arthritis.

In line with this we found that joint inflammation in FcγRI,II,III,IV -/- was much lower when compared with FcγI/II/III-/- and remained at the same level as their WT controls, implying an active role of FcγRIV in inflammation during the chronic phase. The amount of PG depletion in FcγRI,II,III,IV -/-was comparable to that observed in WT. In contrast erosion of cartilage matrix but also bone were found to be significantly lower when compared to WT controls (76% and 34% lower respectively).

Conclusion

Activatory  FcγRIV is crucial in regulating joint inflammation during acute and chronic phase of AIA and became crucial in mediating cartilage and bone destruction during the chronic phase of the disease.


Disclosure:

I. Di Ceglie,
None;

A. Blom,
None;

S. Verbeek,
None;

P. van der Kraan,
None;

W. van den Berg,
None;

P. L. van Lent,
None.

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

« Back to 2014 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/activatory-fc-gamma-receptor-iv-plays-a-crucial-role-in-pathogenesis-of-experimental-immune-complex-mediated-chronic-arthritis/

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