Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Interfacing T-cell effector and regulatory function through CD137 (4-1BB) co-stimulation.

Lara M Myers1, Anthony T Vella

  • 1Department of Immunology, School of Medicine, University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT 06032, USA.

Trends in Immunology
|June 28, 2005
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Endothelial Elavl1 Is Required for CD8 T-Cell Persistence in Atherosclerosis.

Arteriosclerosis, thrombosis, and vascular biology·2026
Same author

Endothelial PTBP1 Deletion in Transplanted Cardiac Tissue Limits Cardiac Allograft Vasculopathy.

bioRxiv : the preprint server for biology·2026
Same author

Dissection of amino acid acquisition pathways demonstrates that amino acid starvation of Borrelia burgdorferi results in a (p)ppGpp-independent maladaptive response.

Communications biology·2025
Same author

Dissection of amino acid acquisition pathways in <i>Borrelia burgdorferi</i> uncovers unique physiological responses.

bioRxiv : the preprint server for biology·2025
Same author

CFTR dictates monocyte adhesion by facilitating integrin clustering but not activation.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

Nanoscopy reveals integrin clustering reliant on kindlin-3 but not talin-1.

Cell communication and signaling : CCS·2025

Co-stimulation is key for T-cell activation, but new findings show it can also induce tolerance. This review explores CD137 (4-1BB) and its dual role in T-cell responses, impacting cancer and autoimmune disease treatments.

Area of Science:

  • Immunology
  • Cellular Biology
  • Clinical Research

Background:

  • Co-stimulation traditionally viewed as essential for T-cell activation.
  • Lack of co-stimulation leads to peripheral T-cell tolerance (unresponsiveness or apoptosis).
  • Emerging evidence suggests co-stimulation can paradoxically induce tolerance.

Purpose of the Study:

  • Reconcile conflicting findings on co-stimulation's role in T-cell activation and tolerance.
  • Focus on CD137 (4-1BB) as a modulator of T-cell responses.
  • Propose a mechanism for CD137-mediated dual function in T-cells.

Main Methods:

  • Review of existing literature on T-cell co-stimulation and CD137.
  • Proposed mechanistic model for CD137 function.
  • Analysis of implications for clinical trials involving T-cell modulation.

Related Experiment Videos

Main Results:

  • CD137-primed CD8 T cells exhibit effector functions.
  • These CD8 T cells also inhibit CD4 T-cell activation.
  • A unified model where CD8 T cells possess both effector and regulatory capacities.

Conclusions:

  • CD137 plays a critical role in balancing T-cell activation and tolerance.
  • CD8 T cells can simultaneously exert anti-tumor effects and regulatory functions.
  • Understanding CD137's mechanism impacts strategies for treating cancer and autoimmune diseases.