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

CD69-induced monocyte apoptosis involves multiple nonredundant signaling pathways

R Ramírez1, J Carracedo, M Castedo

  • 1Unidad de Investigación, Hospital Reina Sofía, Córdoba, Spain.

Cellular Immunology
|September 15, 1996
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

Correction: The tumor suppressor protein PML controls apoptosis induced by the HIV-1 envelope.

Cell death and differentiation·2026
Same author

Impaired autophagy increases susceptibility to endotoxin-induced chronic pancreatitis.

Cell death & disease·2020
Same author

The negative impact of antibiotics on outcomes in cancer patients treated with immunotherapy: a new independent prognostic factor?

Annals of oncology : official journal of the European Society for Medical Oncology·2019
Same author

Microvesicles: ROS scavengers and ROS producers.

Journal of extracellular vesicles·2019
Same author

T-cell bispecific antibodies in node-positive breast cancer: novel therapeutic avenue for MHC class I loss variants.

Annals of oncology : official journal of the European Society for Medical Oncology·2019
Same author

MDM2-TP53 Crossregulation: An Underestimated Target to Promote Loss of TP53 Function and Cell Survival.

Trends in cancer·2018
Same journal

Corrigendum to "Lipophilic recombinant-protein insertion endows lymphocytes with enhanced targeting-infiltration ability in EGFR positive cancer" [Cell. Immunol. 365 (2021) 104376].

Cellular immunology·2026
Same journal

Retraction notice to "Myeloid-derived suppressor cells accumulate in the liver site after sepsis to induce immunosuppression" Cellular Immunology 279 (2012) 12-20.

Cellular immunology·2026
Same journal

The uptake, intracellular trafficking and recycling of FcRn-blocking therapeutics in human endothelial cells in vitro.

Cellular immunology·2026
Same journal

Exosome-mediated immune modulation in rheumatoid arthritis and its role in synovial inflammation and autoimmune amplification.

Cellular immunology·2026
Same journal

Persistent CD4<sup>+</sup> T cell hyporesponsiveness during recovery from prolonged symptomatic SARS-CoV-2 infection.

Cellular immunology·2026
Same journal

Deficit in blood MAIT cells, altered cytokines and T cell dynamics in patients with coronary artery disease.

Cellular immunology·2026
See all related articles

Simultaneous stimulation of monocytes/macrophages with LPS and anti-CD69 triggers apoptosis through three independent pathways: arachidonic acid metabolism, nitric oxide (NO) generation, and pertussis toxin (PTX)-sensitive events, each crucial for cell death.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Signaling

Background:

  • Human monocytes/macrophages and THP1 cells undergo apoptosis when stimulated with lipopolysaccharide (LPS) and anti-CD69 antibody.
  • Activation-induced apoptosis in myelomonocytic cells is a complex process involving multiple signaling pathways.

Purpose of the Study:

  • To elucidate the independent signaling pathways involved in LPS/anti-CD69-induced apoptosis in monocytes/macrophages.
  • To determine the necessity and sufficiency of individual signaling components in apoptosis induction.

Main Methods:

  • Inhibition of phospholipase A2, lipoxygenase, nitric oxide (NO) generation, and pertussis toxin (PTX)-sensitive G-protein signaling.
  • Assessment of apoptosis induction, TNF production, NO generation, and arachidonic acid metabolism.

Related Experiment Videos

  • Utilizing PTX and a catalytically inactive mutant toxin (mPTX) to dissect signaling roles.
  • Main Results:

    • Inhibitors of phospholipase A2, lipoxygenase, and PTX, as well as NO generation inhibition, all prevent apoptosis.
    • These three pathways (arachidonic acid metabolism, NO, and PTX-sensitive events) are independent, as interventions in one do not affect the others.
    • LPS and anti-CD69 alone activate cells but do not induce apoptosis; all three pathways are necessary but insufficient individually.

    Conclusions:

    • Apoptosis induction by LPS/anti-CD69 requires the coordinated action of at least three distinct and independent signaling pathways.
    • These findings highlight the intricate regulation of activation-induced apoptosis in monocytes and macrophages.