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: 1746

Involvement of IL-17-Producing MAIT Cells in the Pathogenesis of Rheumatoid Arthritis

Eri Hayashi1, Asako Chiba2, Mie Kitagaichi3, Kurisu Tada3, Ken Yamaji4, Naoto Tamura1, Yoshinari Takasaki3 and Sachiko Miyake2, 1Rheumatology, Juntendo University School of Medicine, Tokyo, Japan, 2Immunology, Juntendo University School of Medicine, Tokyo, Japan, 3Department of Rheumatology, Juntendo University School of Medicine, Tokyo, Japan, 4Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Chemokine Receptors, interleukins (IL), mucosal T cells and rheumatoid arthritis (RA)

  • Tweet
  • Email
  • Print
Session Information

Title: T cell Biology in Rheumatoid Arthritis and Other Arthritis

Session Type: Abstract Submissions (ACR)

Background/Purpose: Mucosal-associated invariant T (MAIT) cells are a subset of innate-like lymphocytes which are restricted by the MHC-related molecule-1 (MR1) and express a semi-invariant TCRα chain: Vα7.2-Jα33 in humans and Vα19-Jα33 in mice. Previously, our group has reported that murine MAIT cells produced high levels of IL-17 and exacerbated arthritis by enhancing inflammatory responses by using animal models of arthritis. Recent studies have revealed that MAIT cells are abundant in humans. MAIT cells constitute about 5-10% of abT cells in peripheral blood and intestine, suggesting that MAIT cells may play important roles in human autoimmune diseases. In this study, we aimed to investigate whether MAIT cells are involved in the pathogenesis of rheumatoid arthritis (RA).

Methods: Peripheral blood mononuclear cells(PBMC) of RA patients and age- and sex- matched healthy subjects were separated by Lymphoprep. PBMC were stained with anti-human monoclonal antibodies against CD3, γδTCR, Vα7.2TCR, and CD161, and MAIT cells were identified as CD3+γδTCR–Vα7.2TCR+CD161 high cells by FACS. The expression of HLA-DR and CCR9 on MAIT cells and other T cell subsets were also assessed. PBMC (2 x 106 cells per well in 96-well culture plates) were stimulated with phorbol-myristate-acetate (50ng/ml) and ionomycin (500ng/ml) for 3 hours. Breferdin A was added in the last 2 hours of culture. After surface staining, cells were permeabilized by using BD Cytofix/Cytoperm Fixation/Permeabilization Solution Kit and intracellular cytokine staining for IL-17A, IFNγ, TNFα and IL-6 was performed. Cells were analyzed on FACS LSR Fortessa with Flowjo softwere.

Results: The percentages of MAIT cells were decreased in RA patients compared with healthy controls. The reduction in MAIT cell frequency was more enhanced in RA patients with active disease. There was a tendency of increased HLA-DR expression on MAIT cells from patients with lower MAIT cell frequencies. MAIT cells produced IL-17A , IFNγ, TNFα and IL-6 upon stimulation, and the frequency of IL-17A-producing MAIT cells was inversely correlated with that of MAIT cells in RA.  However, there was no correlation with the frequencies of IFNγ-, TNFα- or IL-6- producing cells and that of MAIT cells. We also found the negative correlations in the frequency of a gut-homing chemokine receptor CCR9-positive MAIT cells with that of MAIT cells in RA. 

Conclusion: We demonstrated that the frequency of MAIT cells was reduced in RA. The elevated expression of HLA-DR and IL-17 production by MAIT cells indicated the activated state of remaining MAIT cells in RA. The increase of CCR9-positive MAIT cells indicates the recruitment of gut MAIT cells to the peripheral blood in RA.


Disclosure:

E. Hayashi,
None;

A. Chiba,
None;

M. Kitagaichi,
None;

K. Tada,
None;

K. Yamaji,
None;

N. Tamura,
None;

Y. Takasaki,
None;

S. Miyake,
None.

  • Tweet
  • Email
  • Print

« Back to 2014 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/involvement-of-il-17-producing-mait-cells-in-the-pathogenesis-of-rheumatoid-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