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: 958

Identification of IFN-γ-producing Effector B Cells in Humans: Their Relevance to the Pathogenesis of Systemic Lupus Erythematosus

Kazuhiko Higashioka1, Masahiro Ayano 2, Yasutaka Kimoto 3, Hiroki Mitoma 2, Mitsuteru Akahoshi 2, Yojiro Arinobu 2, Koichi Akashi 1, Takahiko Horiuchi 4 and Hiroaki Niiro 5, 1Department of Medicine and Biosystemic Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan, 2Department of Medicine and Biosystemic Science, Graduate School of Medical Sciences, Fukuoka, Japan, Fukuoka, Japan, 3Department of Internal Medicine, Kyushu University Beppu Hospital, Beppu, Japan, 4Department of Internal Medicine, Kyushu University Beppu Hospital, Beppu, Japan, Beppu, Japan, 5Clinical Education Centre, Kyushu University Hospital, Fukuoka, Japan, Fukuoka, Japan

Meeting: 2019 ACR/ARP Annual Meeting

Keywords: B cells, interferons, systemic lupus erythematosus (SLE) and cytokines

  • Tweet
  • Email
  • Print
Session Information

Date: Monday, November 11, 2019

Title: B Cell Biology & Targets In Autoimmune & Inflammatory Disease Poster

Session Type: Poster Session (Monday)

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

Background/Purpose: Systemic lupus erythematosus (SLE) is an autoimmune, multi-systemic disease that potentially affects any organ in the body. Clinical efficacy of B cell-targeting therapy underscores a crucial role of the antibody (Ab)-independent functions of B cells in the pathogenesis of SLE. Among such functions, cytokine production by B cells has recently gained much attention. The type 2 interferon IFN-γ is a key cytokine involved in SLE and produced by a variety of immune cells, however it remains somewhat elusive whether human B cells have potential to produce this cytokine. Here, we have sought to identify IFN-γ-producing B cells in humans and investigate their role in the pathogenesis of SLE.

Methods: B cell subsets from peripheral blood (PB) from healthy controls (HC) and patients with SLE were enriched by cell sorting, stimulated with CD4+ T cell-related cytokines and subjected to the analysis of IFN-γ expression at both mRNA and protein levels. To check whether IFN-γ-producing B cells can be induced by CD4+ T cells, we co-cultured B cells with CD4+ T cell subsets. To determine the functional impacts of IFN-γ-producing B cells on CD4+ T cells, B cells from patients with SLE were co-cultured with CD4+ T cells. In addition, we thoroughly analyzed the surface markers of IFN-γ-producing B cells in HCPB and investigated whether this unique B cell subset coexists with CD4+ T cell subsets in the effusion of SLE patients with pleuritis.

Results: Among a panel of CD4+ T cell-related cytokines, IFN-γ and IL-21 significantly facilitated the generation of IFN-γ-producing B cells particularly from switched-memory (IgD–CD27+) B cells.In the presence of anti-BCR/CD40L with IFN-γ and IL-21 which mimics stimulation of B cells by follicular helper CD4+ type 1 cells (Tfh1 cells), the CXCR3+ fraction of switched-memory B cells strongly produced IFN-γ. Consistent with this, circulating Tfh1 cells from HCPB induced IFN-γ production from CXCR3+ switched-memory B cells. IFN-γ-producing B cells were enriched in the CD226+PD-1+ fraction. The frequency of CXCR3+ switched-memory B cells was higher in patients with SLE than HC. Intriguingly, under Tfh1 conditions CXCR3+ switched-memory B cells from patients with SLE further accelerated IFN-γ production from CD4+ T cells. In the effusion of SLE patients with pleuritis, Tfh1 cells were the predominant Tfh subset and CD226+PD-1+CXCR3+ switched-memory B cells produced high amounts of IFN-γ.

Conclusion: Together, these findings clearly suggest the existence of IFN-γ-producing effector B cells in humans that are involved in the pathogenesis of SLE via closely interacting with CD4+ T cells.


Disclosure: K. Higashioka, None; M. Ayano, None; Y. Kimoto, None; H. Mitoma, None; M. Akahoshi, None; Y. Arinobu, None; K. Akashi, None; T. Horiuchi, None; H. Niiro, None.

To cite this abstract in AMA style:

Higashioka K, Ayano M, Kimoto Y, Mitoma H, Akahoshi M, Arinobu Y, Akashi K, Horiuchi T, Niiro H. Identification of IFN-γ-producing Effector B Cells in Humans: Their Relevance to the Pathogenesis of Systemic Lupus Erythematosus [abstract]. Arthritis Rheumatol. 2019; 71 (suppl 10). https://acrabstracts.org/abstract/identification-of-ifn-%ce%b3-producing-effector-b-cells-in-humans-their-relevance-to-the-pathogenesis-of-systemic-lupus-erythematosus/. Accessed .
  • Tweet
  • Email
  • Print

« Back to 2019 ACR/ARP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/identification-of-ifn-%ce%b3-producing-effector-b-cells-in-humans-their-relevance-to-the-pathogenesis-of-systemic-lupus-erythematosus/

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