Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
  • Clinical Research and Public Health
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Video Abstracts
  • Reviews
    • View all reviews ...
    • Pancreatic Cancer (Jul 2025)
    • Complement Biology and Therapeutics (May 2025)
    • Evolving insights into MASLD and MASH pathogenesis and treatment (Apr 2025)
    • Microbiome in Health and Disease (Feb 2025)
    • Substance Use Disorders (Oct 2024)
    • Clonal Hematopoiesis (Oct 2024)
    • Sex Differences in Medicine (Sep 2024)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Clinical Research and Public Health
    • Research Letters
    • Letters to the Editor
    • Editorials
    • Commentaries
    • Editor's notes
    • Reviews
    • Viewpoints
    • 100th anniversary
    • Top read articles

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Video Abstracts
  • In-Press Preview
  • Clinical Research and Public Health
  • Research Letters
  • Letters to the Editor
  • Editorials
  • Commentaries
  • Editor's notes
  • Reviews
  • Viewpoints
  • 100th anniversary
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
STALing B cell responses with CD22
Craig P. Chappell, Edward A. Clark
Craig P. Chappell, Edward A. Clark
Published June 3, 2013
Citation Information: J Clin Invest. 2013;123(7):2778-2780. https://doi.org/10.1172/JCI69670.
View: Text | PDF
Commentary

STALing B cell responses with CD22

  • Text
  • PDF
Abstract

Suppressing unwanted humoral immune responses without compromising the host’s ability to respond to foreign pathogens is a primary goal for therapies aimed at ameliorating harmful autoantibody production. Global suppression of the immune system via lymphocyte depletion and/or immunosuppressive drugs can have off-target effects, a limitation to conventional therapies. In this issue of the JCI, Macauley and colleagues utilize a novel platform to inhibit antigen-specific antibody production that preserves the immune system’s ability to respond to unrelated antigens.

Authors

Craig P. Chappell, Edward A. Clark

×

Figure 1

Multiple cellular and molecular targets for modulating Ag-specific B cell responses.

Options: View larger image (or click on image) Download as PowerPoint
Multiple cellular and molecular targets for modulating Ag-specific B cel...
Schematic of methods to achieve Ag-specific vs. nonspecific B cell activation or inhibition. STALs directly induce Ag-specific B cell tolerance by simultaneously targeting Ag to the BCR together with inhibitory signals delivered by CD22 ligands. Alternatively, delivery of Ag to the BCR together with CD180 crosslinking results in Ag-specific B cell activation and Ab production. B cell responses may also be modulated by Ag delivery to receptors found on DC subsets. Ag targeted to SIGLEC-H or BDCA2 found on pDCs indirectly inhibits B cell responses via inhibition of effector CD4+ T cell activation, whereas Ag-specific B cell responses can be induced by delivering Ag to certain C-type lectin receptors found on myeloid DCs. B cell responses can be enhanced or inhibited by nonspecific agents such as TLR agonists or immunosuppressive drugs, respectively.

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts