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: 969

ß-adrenergic Receptor Activation: A Way to Enhance CD4 T Cell Suppression by Improving Regulatory B Cell Function

Nadine Honke1, Birgit Opgenoorth 1, Matthias Schneider 2 and Georg Pongratz 3, 1Department of Rheumatology, Hiller Research Center of Rheumatology, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany, 2Policlinic for Rheumatology & Hiller Research Centre for Rheumatology, Heinrich-Heine-University Duesseldorf, Düsseldorf, Germany, 3Policlinic and Hiller Research Unit of Rheumatology, UKD, Heinrich Heine University, Düsseldorf, Germany

Meeting: 2019 ACR/ARP Annual Meeting

Keywords: B cells, T cells and catecholamines

  • 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, 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:

  1. Rheumatoid arthritis (RA) is an autoimmune disease in which next to other cell populations CD4 T cells play a crucial role. It has been shown that catecholamines provided by the sympathetic nervous system (SNS) ameliorate the development and course of arthritis by increasing the production of the anti-inflammatory cytokine IL-10 in regulatory B cells (Bregs). In the current study, we investigated whether Bregs have the ability to produce catecholamines and how such a production is regulated. Moreover, we tested which adrenergic receptor activation is important to improve the Bregs function to evaluate if an additional adrenergic receptor stimulus can enhance the suppression of CD4 T cells.

Methods:

  • In in vitro experiments on activated murine B cells or B cells and splenocytes from collagen-induced arthritis (CIA) mice, modulation of Bregs and their effect on CD4 T cells proliferation were investigated. The production and release of catecholamines were analyzed in naïve, IgM, CpG or IgM/CpG activated B cells after 4h and 24h by FACS. For analysis of CD4 T cell suppression pre-inactivated or pre-activated B cells and CD3/CD28 activated splenocytes from immunized mice were cocultured for 48h and 72 h. CD4 T cell proliferation as well as the expression of PDL-1 and Fas-L on B cells was monitored by FACS. The IL-10 production from B cells was directly measured in the cells by intracellular FACS staining or in the supernatant of B cell cultures by ELISA.

Results: Catecholamines are not only provided by the SNS but are produced by the B cells themselves. Analysis of B cells by FACS showed a raised production of catecholamines after short time exposure to different B cell activation stimuli (Control vs. IgM, n=6, n.s.; Control vs. CpG, n=6, p***< 0,0002; Control vs. IgM/CpG, n= 6, p****< 0,0001). Long time activation of B cells, on the other hand, leads to release of produced catecholamines (Control vs. IgM, n=4, p**< 0,0029; Control vs. CpG, n=4, p****< 0,0001; Control vs. IgM/CpG, n= 4, p****< 0,0001). This hints to a time and context dependent production and release of catecholamines. Furthermore, FACS analysis showed that CpG-activated Bregs have the ability to suppress CD4 T cells (Control vs. CpG, n= 11, p****< 0,0001). Increased suppression of CD4 T cells was observed after addition of norepinephrine or isoproterenol, ADR beta agonists, to CpG-activated Bregs (CpG vs. CpG/NE, n=11, p*=0,0343; CpG vs. CpG/Iso, n=11, p***=0,0009). This higher suppression of CD4 T cells correlates with enhanced IL-10 production by Bregs (CpG vs. CpG+Iso, n=8, % rel. to control ~40%, p**=0,0045; CpG vs. CpG+NE, n=8, % rel. to control ~16%, p**=0,0012).

Conclusion: In conclusion, our data suggest that ß-adrenergic receptor activation by catecholamines or synthethic receptor agonists in addition to a BCR/TLR9 stimulus is associated with an increase of the anti-inflammatory potential of regulatory B cells to suppress CD4 T cells. This could be a strategy to modulate Bregs for therapeutic purposes in RA.


Disclosure: N. Honke, None; B. Opgenoorth, None; M. Schneider, None; G. Pongratz, None.

To cite this abstract in AMA style:

Honke N, Opgenoorth B, Schneider M, Pongratz G. ß-adrenergic Receptor Activation: A Way to Enhance CD4 T Cell Suppression by Improving Regulatory B Cell Function [abstract]. Arthritis Rheumatol. 2019; 71 (suppl 10). https://acrabstracts.org/abstract/s-adrenergic-receptor-activation-a-way-to-enhance-cd4-t-cell-suppression-by-improving-regulatory-b-cell-function/. 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 2019 ACR/ARP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/s-adrenergic-receptor-activation-a-way-to-enhance-cd4-t-cell-suppression-by-improving-regulatory-b-cell-function/

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