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: 302

From Monocytes to Macrophages:  the Pathogeneses of Spontaneous Inflammatory Arthritis in CD11c-Flip-KO (HUPO) Mice

Qi Quan Huang1, Renee E. Doyle2, Philip J. Homan1, Harris Perlman3, Deborah R. WInter3 and Richard M. Pope2, 1Division of Rheumatology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, 2Medicine/Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, 3Department of Medicine Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL

Meeting: 2017 ACR/ARHP Annual Meeting

Date of first publication: September 18, 2017

Keywords: Arthritis, inflammation and monocytes, Macrophage, RNA

  • 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: Sunday, November 5, 2017

Title: Innate Immunity and Rheumatic Disease Poster I

Session Type: ACR Poster Session A

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

Background/Purpose:

We have generated a CD11c-Flip-KO mouse line (HUPO) that spontaneously develops erosive arthritis with incidence 70-80% at age ≥ 20 weeks. This study aimed at understanding the role of monocytes in HUPO arthritis and to define the molecular changes during differentiation to macrophages in the inflamed joint compared with controls.

Methods:

Arthritis was evaluated by clinical score. Cell types from blood and ankle joints are determined by flow cytometry. Cell proliferation are determined by BrdU incorporation and populations of cells were isolated for RNAseq.

Results:

Circulating monocytes, defined as CD45+CD11b+CD115+F4/80lo, were further characterized as classical (CM), Ly6C+CD62L+, or non-classical (NCM), Ly6C–CD62L–. CM were markedly increased in HUPO mice with arthritis and positively correlated with arthritis severity. 70 -90% of CM are also CCR2+ in HUPO mice with arthritis, similar to that in control mice. In contrast, in the HUPO mice without arthritis, only 0-7% of these cells are CCR2+, and the CM numbers were normal. Monocytes recently recruited into synovium are defined as CD45+Ly6C+CD64+CD11b+F4/80intLy6C+MHCII–. This population demonstrated reduced CD115 and increase F4/80 compared with CMs. Within 24 hours after BrdU injection, in both HUPO and control mice, >60% of these Ly6C+MHCII– macrophages incorporated BrdU, comparable to CM and bone marrow monocytes. In contrast, < 1% in NCM incorporated BrdU. In HUPO mice during further differentiation the macrophages became Ly6C+MHCII+ and then Ly6C–MHCII+, with less BrdU incorporation in the more differentiated cells. A similar transition was observed in the control mice except the Ly6C+MHCII+ population was not identified. CMs and F4/80int macrophages were isolated for RNAseq. In the controls, clusters of differentially expressed genes were identified in CMs, and Ly6C+MHCII– and Ly6C–MHCII+ joint macrophages. For example Immune response and leukocyte activation were increase in CMs while cell cycle and cell division were increased in Ly6C+MHCII– macrophages. There were differences in these transcriptional profiles of the macrophages subset between HUPO and control mice, including those regulating cell cycle and differentiation as well as for monocyte differentiation and antigen processing.

Conclusion:

These observations demonstrate that during chronic inflammation, CMs enter the joints and undergo macrophage differentiation during homeostasis and chronic inflammation. The differences in transcriptional profiles between the control and HUPO mice will provide important insights into the mechanisms contributing to chronic inflammation.


Disclosure: Q. Q. Huang, None; R. E. Doyle, None; P. J. Homan, None; H. Perlman, None; D. R. WInter, None; R. M. Pope, None.

To cite this abstract in AMA style:

Huang QQ, Doyle RE, Homan PJ, Perlman H, WInter DR, Pope RM. From Monocytes to Macrophages:  the Pathogeneses of Spontaneous Inflammatory Arthritis in CD11c-Flip-KO (HUPO) Mice [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/from-monocytes-to-macrophages-the-pathogeneses-of-spontaneous-inflammatory-arthritis-in-cd11c-flip-ko-hupo-mice/. 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 2017 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/from-monocytes-to-macrophages-the-pathogeneses-of-spontaneous-inflammatory-arthritis-in-cd11c-flip-ko-hupo-mice/

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