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

The cytolytic C5b-9 complement complex: feedback inhibition of complement activation.

S Bhakdi1, F Maillet, M Muhly

  • 1Institute of Medical Microbiology, Giessen, Federal Republic of Germany.

Proceedings of the National Academy of Sciences of the United States of America
|March 1, 1988
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

[Enteroviral infections in adults treated with rituximab: A new case of chronic meningitis and myofasciitis and literature review].

La Revue de medecine interne·2020
Same author

Lactobacillus delbrueckii urinary tract infection in a male patient.

Medecine et maladies infectieuses·2018
Same author

Intravenous immunoglobulin and immune response.

Clinical and experimental immunology·2014
Same author

[Surgical complications in kidney transplantation].

Annales d'urologie·2008
Same author

Late ureteral stenosis following renal transplantation: risk factors and impact on patient and graft survival.

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons·2006
Same author

Immunomodulation of autoimmune and inflammatory diseases with intravenous immunoglobulin.

Clinical and experimental medicine·2005

The terminal complement complex (C5b-9(m)) regulates complement activity by inhibiting C3 convertase formation and C5 utilization. This feedback inhibition mechanism controls complement effector functions, including bacterial lysis and erythrocyte hemolysis.

Area of Science:

  • Immunology
  • Complement System Biology

Background:

  • The complement system is a crucial part of innate immunity.
  • The terminal complement pathway culminates in the formation of the membrane attack complex (MAC), C5b-9(m).
  • The regulatory mechanisms of C5b-9(m) function are not fully understood.

Purpose of the Study:

  • To investigate the regulatory role of the terminal cytolytic C5b-9 complex (C5b-9(m)) in human complement.
  • To determine the impact of C5b-9(m) on complement-mediated lysis and effector functions.

Main Methods:

  • Isolation and purification of C5b-9(m) complexes from target membranes.
  • In vitro assays using sensitized sheep erythrocytes and human serum.
  • Experiments with purified complement components and modified SC5b-9 complexes.

Related Experiment Videos

  • Assessment of bactericidal activity against Escherichia coli and hemolytic activity against autologous erythrocytes.

    • Main Results:

    • Purified C5b-9(m) inhibited complement-mediated lysis of erythrocytes in a dose-dependent manner.
    • C5b-7 and C5b-8 complexes also exhibited inhibitory function, indicating C9 is not essential.
    • The fluid-phase SC5b-9 complex was inactive, but tryptic modification conferred inhibitory capacity.
    • C5b-9(m) regulated the formation of classical and alternative pathway C3 convertases and C5 convertase activity.
    • C5b-9(m) abolished the bactericidal effect of serum on E. coli and suppressed its hemolytic function.

    Conclusions:

    • The terminal cytolytic C5b-9 complex (C5b-9(m)) possesses a significant regulatory function within the human complement system.
    • C5b-9(m) acts as a feedback inhibitor, modulating key steps in complement activation pathways.
    • This autoregulatory mechanism is biologically relevant for controlling complement effector functions, preventing excessive damage.