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

Membrane signaling by complement C5b-9, the membrane attack complex

A Nicholson-Weller1, J A Halperin

  • 1Department of Medicine, Brigham and Women's Hospital, Boston, Mass.

Immunologic Research
|January 1, 1993
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

The future of compounding: an industry perspective.

International journal of pharmaceutical compounding·2013
Same author

Glycated-CD59 antigen: exploration of synthetic approaches.

Advances in experimental medicine and biology·2009
Same author

Antibody CR1-2B11 recognizes a non-polymorphic epitope of human CR1 (CD35).

Clinical and experimental immunology·2007
Same author

Analysis of the promoters and 5'-UTR of mouse Cd59 genes, and of their functional activity in erythrocytes.

Genes and immunity·2006
Same author

C5L2 receptor is not involved in C3a / C3a-desArg-mediated enhancement of bone marrow hematopoietic cell migration to CXCL12.

Leukemia·2005
Same author

A transgenic mouse model for studying the clearance of blood-borne pathogens via human complement receptor 1 (CR1).

Clinical and experimental immunology·2005
Same journal

Immunological spectrum in patients with thymoma: beyond good syndrome.

Immunologic research·2026
Same journal

Microbiome immune crosstalk in Sjögren's syndrome: mechanistic insights and translational perspectives.

Immunologic research·2026
Same journal

Immune checkpoint inhibitor-induced myasthenia gravis and myocarditis: a fatal immune-related adverse event.

Immunologic research·2026
Same journal

TRIM28 and TRIM32: multifaceted regulators of innate immunity and antiviral defence.

Immunologic research·2026
Same journal

Decoding PANoptosis: Crosstalk of cell death pathways in immunity and inflammation.

Immunologic research·2026
Same journal

Comment on "Anti-neutrophil cytoplasmic antibodies in interstitial lung disease: results from a cross-sectional study and meta-analysis".

Immunologic research·2026
See all related articles

Terminal complement complexes (TCCs) like C5b-9 trigger nonlethal cell signals, including calcium influx. These complexes are crucial in inflammatory processes, as shown by the absence of inflammation in complement-deficient models.

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Terminal complement complexes (TCCs), including C5b-7, C5b-8, and C5b-9, are key effectors of the complement system.
  • These complexes can initiate intracellular signaling pathways within target cells.
  • TCCs are implicated in various inflammatory conditions.

Purpose of the Study:

  • To investigate the nonlethal signaling capabilities of TCCs.
  • To elucidate the role of TCCs in cellular responses and inflammation.

Main Methods:

  • Analysis of cell signaling events triggered by TCCs (C5b-8, C5b-9).
  • Measurement of intracellular calcium (Ca2+) influx.
  • Detection of other second messengers like cAMP and inositol phosphates.
  • Utilizing complement-deficient animal models to assess inflammation.

Related Experiment Videos

Main Results:

  • TCCs, specifically C5b-8 and C5b-9, induce nonlethal cellular signals.
  • A universal consequence is an influx of Ca2+.
  • Specific cell types exhibit generation of other second messengers (cAMP, inositol phosphates, arachidonate metabolites).
  • In vivo studies show TCCs in diverse inflammatory processes.
  • Complement-deficient models demonstrate a lack of inflammation, confirming TCCs' role.

Conclusions:

  • TCCs are potent inducers of nonlethal cellular signaling pathways.
  • The Ca2+ influx is a common cellular response to TCCs.
  • TCCs play a critical role in the pathogenesis of inflammatory lesions.