Skip to main content

Main menu

  • Home
  • Articles
    • Current Issue
    • Next in The JI
    • Archive
    • Brief Reviews
    • Pillars of Immunology
    • Translating Immunology
    • Most Read
    • Top Downloads
    • Annual Meeting Abstracts
  • COVID-19/SARS/MERS Articles
  • Info
    • About the Journal
    • For Authors
    • Journal Policies
    • Influence Statement
    • For Advertisers
  • Editors
  • Submit
    • Submit a Manuscript
    • Instructions for Authors
    • Journal Policies
  • Subscribe
    • Journal Subscriptions
    • Email Alerts
    • RSS Feeds
    • ImmunoCasts
  • More
    • Most Read
    • Most Cited
    • ImmunoCasts
    • AAI Disclaimer
    • Feedback
    • Help
    • Accessibility Statement
  • Other Publications
    • American Association of Immunologists
    • ImmunoHorizons

User menu

  • Subscribe
  • Log in

Search

  • Advanced search
The Journal of Immunology
  • Other Publications
    • American Association of Immunologists
    • ImmunoHorizons
  • Subscribe
  • Log in
The Journal of Immunology

Advanced Search

  • Home
  • Articles
    • Current Issue
    • Next in The JI
    • Archive
    • Brief Reviews
    • Pillars of Immunology
    • Translating Immunology
    • Most Read
    • Top Downloads
    • Annual Meeting Abstracts
  • COVID-19/SARS/MERS Articles
  • Info
    • About the Journal
    • For Authors
    • Journal Policies
    • Influence Statement
    • For Advertisers
  • Editors
  • Submit
    • Submit a Manuscript
    • Instructions for Authors
    • Journal Policies
  • Subscribe
    • Journal Subscriptions
    • Email Alerts
    • RSS Feeds
    • ImmunoCasts
  • More
    • Most Read
    • Most Cited
    • ImmunoCasts
    • AAI Disclaimer
    • Feedback
    • Help
    • Accessibility Statement
  • Follow The Journal of Immunology on Twitter
  • Follow The Journal of Immunology on RSS

Reactive Oxidative Species–Modulated Ca2+ Release Regulates β2 Integrin Activation on CD4+ CD28null T Cells of Acute Coronary Syndrome Patients

Yvonne Samstag, Nicolai V. Bogert, Guido H. Wabnitz, Shabana Din, Markus Therre, Florian Leuschner, Hugo A. Katus and Mathias H. Konstandin
J Immunol October 15, 2020, 205 (8) 2276-2286; DOI: https://doi.org/10.4049/jimmunol.2000327
Yvonne Samstag
*Institute of Immunology, Section Molecular Immunology, Ruprecht-Karls-University, D-69120 Heidelberg, Germany;
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Yvonne Samstag
Nicolai V. Bogert
†Department of Cardiology, Heidelberg University Hospital, Ruprecht-Karls-University, D-69120 Heidelberg, Germany; and
‡German Centre for Cardiovascular Research Partner Site Heidelberg/Mannheim, Germany, Heidelberg University Hospital, D-69120 Heidelberg, Germany
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Guido H. Wabnitz
*Institute of Immunology, Section Molecular Immunology, Ruprecht-Karls-University, D-69120 Heidelberg, Germany;
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Shabana Din
†Department of Cardiology, Heidelberg University Hospital, Ruprecht-Karls-University, D-69120 Heidelberg, Germany; and
‡German Centre for Cardiovascular Research Partner Site Heidelberg/Mannheim, Germany, Heidelberg University Hospital, D-69120 Heidelberg, Germany
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Markus Therre
†Department of Cardiology, Heidelberg University Hospital, Ruprecht-Karls-University, D-69120 Heidelberg, Germany; and
‡German Centre for Cardiovascular Research Partner Site Heidelberg/Mannheim, Germany, Heidelberg University Hospital, D-69120 Heidelberg, Germany
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Florian Leuschner
†Department of Cardiology, Heidelberg University Hospital, Ruprecht-Karls-University, D-69120 Heidelberg, Germany; and
‡German Centre for Cardiovascular Research Partner Site Heidelberg/Mannheim, Germany, Heidelberg University Hospital, D-69120 Heidelberg, Germany
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Hugo A. Katus
†Department of Cardiology, Heidelberg University Hospital, Ruprecht-Karls-University, D-69120 Heidelberg, Germany; and
‡German Centre for Cardiovascular Research Partner Site Heidelberg/Mannheim, Germany, Heidelberg University Hospital, D-69120 Heidelberg, Germany
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Mathias H. Konstandin
†Department of Cardiology, Heidelberg University Hospital, Ruprecht-Karls-University, D-69120 Heidelberg, Germany; and
‡German Centre for Cardiovascular Research Partner Site Heidelberg/Mannheim, Germany, Heidelberg University Hospital, D-69120 Heidelberg, Germany
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF + SI
  • PDF
Loading

Key Points

  • CD28null T cells show high reactivity of β2 integrin upon chemokine stimulation.

  • ROS-mediated Ca2+ release is critical for β2 integrin activation in T cells.

  • Spontaneous β2 integrin activity of CD28null T cells in ACS is ROS dependent.

Abstract

The number and activity of T cell subsets in the atherosclerotic plaques are critical for the prognosis of patients with acute coronary syndrome. β2 Integrin activation is pivotal for T cell recruitment and correlates with future cardiac events. Despite this knowledge, differential regulation of adhesiveness in T cell subsets has not been explored yet. In this study, we show that in human T cells, SDF-1α–mediated β2 integrin activation is driven by a, so far, not-described reactive oxidative species (ROS)–regulated calcium influx. Furthermore, we show that CD4+CD28null T cells represent a highly reactive subset showing 25-fold stronger β2 integrin activation upon SDF-1α stimulation compared with CD28+ T cells. Interestingly, ROS-dependent Ca release was much more prevalent in the pathogenetically pivotal CD28null subset compared with the CD28+ T cells, whereas the established mediators of the classical pathways for β2 integrin activation (PKC, PI3K, and PLC) were similarly activated in both T cell subsets. Thus, interference with the calcium flux attenuates spontaneous adhesion of CD28null T cells from acute coronary syndrome patients, and calcium ionophores abolished the observed differences in the adhesion properties between CD28+ and CD28null T cells. Likewise, the adhesion of these T cell subsets was indistinguishable in the presence of exogenous ROS/H2O2. Together, these data provide a molecular explanation of the role of ROS in pathogenesis of plaque destabilization.

Footnotes

  • The online version of this article contains supplemental material.

  • Abbreviations used in this article:

    ACS
    acute coronary syndrome
    Apo
    apocynin
    DPI
    diphenylene iodonium chloride
    LC-AA
    ligand complex–based adhesion assay
    MFI
    mean fluorescence intensity
    NAC
    N-acetylcysteine
    Ptx
    pertussis toxin
    redox
    oxidation reduction
    RFP
    red fluorescence protein
    roGFP
    redox-sensitive GFP
    ROS
    reactive oxidative species.

  • Received March 28, 2020.
  • Accepted August 17, 2020.
  • Copyright © 2020 by The American Association of Immunologists, Inc.
View Full Text

Pay Per Article - You may access this article (from the computer you are currently using) for 1 day for US$37.50

Regain Access - You can regain access to a recent Pay per Article purchase if your access period has not yet expired.

Log in using your username and password

Forgot your user name or password?
PreviousNext
Back to top

In this issue

The Journal of Immunology: 205 (8)
The Journal of Immunology
Vol. 205, Issue 8
15 Oct 2020
  • Table of Contents
  • Table of Contents (PDF)
  • About the Cover
  • Back Matter (PDF)
  • Editorial Board (PDF)
  • Front Matter (PDF)
Print
Download PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for your interest in spreading the word about The Journal of Immunology.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Reactive Oxidative Species–Modulated Ca2+ Release Regulates β2 Integrin Activation on CD4+ CD28null T Cells of Acute Coronary Syndrome Patients
(Your Name) has forwarded a page to you from The Journal of Immunology
(Your Name) thought you would like to see this page from the The Journal of Immunology web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Reactive Oxidative Species–Modulated Ca2+ Release Regulates β2 Integrin Activation on CD4+ CD28null T Cells of Acute Coronary Syndrome Patients
Yvonne Samstag, Nicolai V. Bogert, Guido H. Wabnitz, Shabana Din, Markus Therre, Florian Leuschner, Hugo A. Katus, Mathias H. Konstandin
The Journal of Immunology October 15, 2020, 205 (8) 2276-2286; DOI: 10.4049/jimmunol.2000327

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
Reactive Oxidative Species–Modulated Ca2+ Release Regulates β2 Integrin Activation on CD4+ CD28null T Cells of Acute Coronary Syndrome Patients
Yvonne Samstag, Nicolai V. Bogert, Guido H. Wabnitz, Shabana Din, Markus Therre, Florian Leuschner, Hugo A. Katus, Mathias H. Konstandin
The Journal of Immunology October 15, 2020, 205 (8) 2276-2286; DOI: 10.4049/jimmunol.2000327
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like

Jump to section

  • Article
    • Abstract
    • Introduction
    • Materials and Methods
    • Results
    • Discussion
    • Disclosures
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • PDF + SI
  • PDF

Related Articles

Cited By...

More in this TOC Section

  • Identification and Characterization of Zebrafish Tlr4 Coreceptor Md-2
  • Activated Neutrophils Propagate Fetal Membrane Inflammation and Weakening through ERK and Neutrophil Extracellular Trap–Induced TLR-9 Signaling
  • Enhanced Proliferation of Ly6C+ Monocytes/Macrophages Contributes to Chronic Inflammation in Skin Wounds of Diabetic Mice
Show more INNATE IMMUNITY AND INFLAMMATION

Similar Articles

Navigate

  • Home
  • Current Issue
  • Next in The JI
  • Archive
  • Brief Reviews
  • Pillars of Immunology
  • Translating Immunology

For Authors

  • Submit a Manuscript
  • Instructions for Authors
  • About the Journal
  • Journal Policies
  • Editors

General Information

  • Advertisers
  • Subscribers
  • Rights and Permissions
  • Accessibility Statement
  • Public Access
  • Privacy Policy
  • Disclaimer

Journal Services

  • Email Alerts
  • RSS Feeds
  • ImmunoCasts
  • Twitter

Copyright © 2021 by The American Association of Immunologists, Inc.

Print ISSN 0022-1767        Online ISSN 1550-6606