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

T cells in glomerulonephritis.

Peter G Tipping1, Stephen R Holdsworth

  • 1Centre for Inflammatory Diseases Monash University, Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria, 3168 Australia.

Springer Seminars in Immunopathology
|June 5, 2003
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

Toll-like Receptor 9 Induced Dendritic Cell Activation Promotes Anti-Myeloperoxidase Autoimmunity and Glomerulonephritis.

International journal of molecular sciences·2023
Same author

Conversion of the Liver into a Biofactory for DNaseI Using Adeno-Associated Virus Vector Gene Transfer Reduces Neutrophil Extracellular Traps in a Model of Systemic Lupus Erythematosus.

Human gene therapy·2022
Same author

Heterologous Immunity Between SARS-CoV-2 and Pathogenic Bacteria.

Frontiers in immunology·2022
Same author

Ageing enhances cellular immunity to myeloperoxidase and experimental anti-myeloperoxidase glomerulonephritis.

Rheumatology (Oxford, England)·2021
Same author

BCG Vaccine Derived Peptides Induce SARS-CoV-2 T Cell Cross-Reactivity.

Frontiers in immunology·2021
Same author

Emerging Cellular Therapies for Anti-myeloperoxidase Vasculitis and Other Autoimmune Diseases.

Frontiers in immunology·2021
Same journal

Antibody and complement-dependent viral neutralization.

Springer seminars in immunopathology·2020
Same journal

Antibody mediated complement dependent lysis of virus infected cells.

Springer seminars in immunopathology·2020
Same journal

Activating and inhibitory FcgammaRs in autoimmune disorders.

Springer seminars in immunopathology·2006
Same journal

Injecting drugs of abuse and immunity: implications for HIV vaccine testing and efficacy.

Springer seminars in immunopathology·2006
Same journal

Fcepsilon- and Fcgamma-receptor signaling in diseases.

Springer seminars in immunopathology·2006
Same journal

Fc gamma receptors and cancer.

Springer seminars in immunopathology·2006
See all related articles

Cellular immunity, particularly T cells, plays a crucial role in glomerulonephritis pathogenesis, influencing disease patterns and outcomes. Understanding T helper cell subsets (Th1/Th2) is key to deciphering immune responses in kidney inflammation.

Area of Science:

  • Immunology
  • Nephrology
  • Pathogenesis of Glomerulonephritis

Background:

  • Humoral immunity (immunoglobulin, complement) is a long-recognized factor in glomerulonephritis.
  • The role of cellular immunity, specifically T cells, is a more recent area of investigation.
  • Distinct T helper cell subsets (Th1 and Th2) mediate different immune responses.

Purpose of the Study:

  • To explore the contribution of cellular immunity and T cells in the immunopathogenesis of glomerulonephritis.
  • To investigate how the balance of T helper cell subsets influences disease patterns and outcomes.
  • To understand the effector role of T cells in specific glomerulonephritis types.

Main Methods:

  • Review of existing literature on immunoglobulin, complement, and T cell involvement in glomerulonephritis.

Related Experiment Videos

  • Analysis of the factors influencing T helper cell subset activation (antigen presentation, cytokine milieu).
  • Examination of T cell prominence in proliferative, crescentic, and anti-neutrophil cytoplasmic antibody-associated glomerulonephritis.

    • Main Results:

    • T cells are increasingly recognized for their significant role in glomerulonephritis.
    • The balance of Th1/Th2 activation impacts effector pathways and injury patterns.
    • T cells are prominent in proliferative and crescentic forms, often with delayed-type hypersensitivity mediators.
    • In anti-neutrophil cytoplasmic antibody-associated glomerulonephritis, T cells are key, even without antibody deposition.

    Conclusions:

    • Cellular immunity, driven by T cells, is a critical determinant of glomerulonephritis immunopathogenesis.
    • The Th1/Th2 balance is vital in directing disease mechanisms and injury.
    • T cells play a pivotal effector role, especially in rapidly progressive forms of glomerulonephritis with poor prognoses.