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: 982

In the Presence of IL-18, IL-10 but Not IL-6 Induces IFN-γ Production and the Surface Expression of TRAIL on NK Cells

Kojiro Sato, Yoshimi Aizaki, Hiroaki Yazawa and Toshihide Mimura, Department of Rheumatology and Applied Immunology, Faculty of Medicine, Saitama Medical University, Saitama, Japan

Meeting: 2018 ACR/ARHP Annual Meeting

Keywords: adult-onset Still's disease and natural killer (NK) cells, IL-1/IL-18, IL-6

  • 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: Monday, October 22, 2018

Title: Cytokines and Cell Trafficking Poster

Session Type: ACR Poster Session B

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

Background/Purpose: Adult-onset Still’s disease (AOSD) is a systemic inflammatory disease, the cause of which is largely unknown. AOSD has been recently classified as one of the autoinflammatory diseases in which innate rather than acquired immunity plays an important role in the pathogenesis. Serum IL-18 has been shown to be high in AOSD patients. In this study, we first quantified the levels of multiple cytokines in the serum of AOSD patients and then compared the cytokine profile with that of healthy controls. We next evaluated the effects of the cytokines detectable in the AOSD serum on natural killer (NK) cells, since NK cells are cells of innate immunity and IL-18 has been shown to enhance their cytotoxicity.

Methods: Our patients fulfilled Yamaguchi’s criteria for the diagnosis of AOSD. We quantified the serum levels of 10 cytokines (IFN-α, IFN-γ, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12p70, IL-17A and TNF-α) using multiplex bead array assays and IL-18 using ELISA. We next sorted NK cells from peripheral blood mononuclear cells of healthy controls and stimulated them in vitro in the presence of cytokines that were detected in the AOSD serum. We quantified the level of IFN-γ in the culture supernatant by ELISA and assessed the surface expression level of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) on NK cells by flow cytometry.

Results: The level of IL-18 was high in all of the AOSD samples. IL-6 was detectable in 8 out of 16 patients and IL-10 in 3 out of 16. In contrast, serum IFN-γ was not detected in any sample. When NK cells were stimulated in vitro with IL-18 alone, IFN-γ was undetectable in the culture supernatant. The combination of IL-10 and IL-18, but not IL-6 and IL-18, induced IFN-γ. We evaluated the expression of the receptors for IL-6 and IL-10 on NK cells and found that IL-10R and IL-10RB were present, while IL-6R and gp130 were absent. The combination of IL-10 and IL-18 also induced TRAIL expression on NK cells.

Conclusion: Since IL-18 was originally identified as an inducer of IFN-γ, it was surprising that IFN-γ was not detected in the serum despite the high level of IL-18. Indeed, IL-18 alone did not induce the production of IFN-γ from NK cells in vitro. The combination of IL-10 and IL-18, but not IL-6 and IL-18, induced the production of IFN-γ and surface expression of TRAIL on NK cells. As IL-6 is a classic pro-inflammatory cytokine and IL-10 is considered anti-inflammatory, this result was also rather unexpected. The unresponsiveness to IL-6 may be explained by the absence of IL-6 receptor on NK cells. Locally-produced IFN-γ can be detrimental to the body by activating macrophages. As the liver is rich in NK cells and TRAIL has been reported to cause liver injury, TRAIL on NK cells may be responsible for one of the characteristics of AOSD, liver dysfunction. Although IL-10 may be produced to prevent excessive inflammation, in the presence of IL-18, it can exert the opposite effect.


Disclosure: K. Sato, None; Y. Aizaki, None; H. Yazawa, None; T. Mimura, None.

To cite this abstract in AMA style:

Sato K, Aizaki Y, Yazawa H, Mimura T. In the Presence of IL-18, IL-10 but Not IL-6 Induces IFN-γ Production and the Surface Expression of TRAIL on NK Cells [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 9). https://acrabstracts.org/abstract/in-the-presence-of-il-18-il-10-but-not-il-6-induces-ifn-%ce%b3-production-and-the-surface-expression-of-trail-on-nk-cells/. 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 2018 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/in-the-presence-of-il-18-il-10-but-not-il-6-induces-ifn-%ce%b3-production-and-the-surface-expression-of-trail-on-nk-cells/

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