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

[Cell cooperation in immune responses]

C Carnaud1

  • 1INSERM U 25, hôpital Necker, Paris.

La Revue Du Praticien
|January 1, 1994
PubMed
Summary
This summary is machine-generated.

Immune responses rely on diverse cell types, including lymphocytes and myeloid cells, working together. This cellular cooperation, mediated by direct contact or soluble factors like cytokines, is crucial for regulating immune functions.

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

Damage control, rather than unresponsiveness, effected by protective DX5+ T cells in autoimmune diabetes.

Nature immunology·2001
Same author

NK T cell-induced protection against diabetes in V alpha 14-J alpha 281 transgenic nonobese diabetic mice is associated with a Th2 shift circumscribed regionally to the islets and functionally to islet autoantigen.

Journal of immunology (Baltimore, Md. : 1950)·2001
Same author

Protection against diabetes and improved NK/NKT cell performance in NOD.NK1.1 mice congenic at the NK complex.

Journal of immunology (Baltimore, Md. : 1950)·2001
Same author

Prion diseases and the immune system.

Clinical immunology (Orlando, Fla.)·2000
Same author

Cutting edge: Cross-talk between cells of the innate immune system: NKT cells rapidly activate NK cells.

Journal of immunology (Baltimore, Md. : 1950)·1999
Same author

Non-obese diabetic (NOD) mice are genetically susceptible to experimental autoimmune prostatitis (EAP).

Journal of autoimmunity·1999
Same journal

[Prolonged fever].

La Revue du praticien·2026
Same journal

[Lower gastrointestinal bleeding].

La Revue du praticien·2026
Same journal

[Management of antiplatelet agents and oral anticoagulants in cases of gastrointestinal bleeding].

La Revue du praticien·2026
Same journal

[A history of child abuse intervention in the West].

La Revue du praticien·2026
Same journal

[Agranulocytose médicamenteuse].

La Revue du praticien·2026
Same journal

[Patient education in heart failure].

La Revue du praticien·2026
See all related articles

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Context:

  • Immune responses involve complex interactions between various immune cell subpopulations.
  • Accessory and helper cells, including lymphocytes and myeloid cells (macrophages, dendritic cells), are essential for immune regulation.
  • Cellular cooperation occurs through direct cell-to-cell contact or indirect signaling via soluble mediators like cytokines.

Purpose:

  • To elucidate the mechanisms of cellular cooperation in immune responses.
  • To highlight the roles of accessory and helper cells in immune regulation.
  • To explore the potential for therapeutic manipulation of immune responses.

Summary:

  • Immune responses are orchestrated by diverse cell subpopulations with complementary functions.

Related Experiment Videos

  • Accessory and helper cells, such as antigen-presenting B cells, helper T cells, macrophages, monocytes, and dendritic cells, collaborate with effector lymphocytes.
  • Cooperation occurs via cell-surface interactions (receptor-ligand) or soluble mediators (cytokines), enabling immune system self-regulation.

    • Impact:

    • Understanding these cellular interactions provides insights into immune system autoregulation.
    • The characterization of surface molecules and cytokines allows for potential therapeutic interventions.
    • Modulating these pathways can amplify beneficial immune signals or suppress detrimental responses.