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 Concept Videos

Cell-mediated Immune Responses01:40

Cell-mediated Immune Responses

86.5K
Overview
86.5K
Frequency-dependent Selection01:21

Frequency-dependent Selection

24.5K
When the fitness of a trait is influenced by how common it is (i.e., its frequency) relative to different traits within a population, this is referred to as frequency-dependent selection. Frequency-dependent selection may occur between species or within a single species. This type of selection can either be positive—with more common phenotypes having higher fitness—or negative, with rarer phenotypes conferring increased fitness.
24.5K
Special Features of Adaptive Immunity01:20

Special Features of Adaptive Immunity

4.5K
The adaptive immune system, a crucial component of the overall immune response, offers a highly specialized defense against pathogens. It involves specific cell types and features, enabling it to combat infections effectively and efficiently.
The primary cell types involved in adaptive immunity are T cells and B cells. Each type has a unique role in defending the body against pathogens. T cells are responsible for cell-mediated immunity. They identify and eliminate infected cells directly,...
4.5K
T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

17.5K
T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...
17.5K
Secondary Lymphoid Organs01:15

Secondary Lymphoid Organs

10.3K
Secondary organs, including lymph nodes, the spleen, and mucosa-associated lymphoid tissue (MALT), work harmoniously to protect us from disease and infection.
The spleen is a vital organ in the lymphatic system, nestled in the upper left side of the abdomen. It is composed of two primary regions: the red pulp and the white pulp, each having distinct functions. The red pulp performs a significant role in blood filtration. It efficiently purges the blood of old or damaged red blood cells and...
10.3K
B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

18.4K
The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
18.4K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Barriers and facilitators to neurodevelopmental follow-up among at-risk newborns across Washington State.

Research square·2026
Same author

Serum proteomic atlas reveals distinct molecular signatures of lupus nephritis activity, chronicity, and treatment response.

bioRxiv : the preprint server for biology·2026
Same author

Spatially Distinct Macrophage Subsets Drive Myofibroblast Heterogeneity and Maladaptive Fibrosis in Lupus Nephritis.

bioRxiv : the preprint server for biology·2026
Same author

Deep profiling of lupus nephritis kidneys reveals dynamic changes in myeloid cells associated with disease progression.

Annals of the rheumatic diseases·2026
Same author

A population-scale atlas of blood and tissue in lupus nephritis.

bioRxiv : the preprint server for biology·2026
Same author

RPS19 and RPL5 haploinsufficient models reveal divergent ribosomal subunit controls of fetal hematopoiesis.

Nature communications·2026

Related Experiment Video

Updated: Apr 4, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
12:04

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

Published on: November 1, 2015

19.1K

Defects in Germinal Center Selection in SLE.

Megan Woods1, Yong-Rui Zou1, Anne Davidson1

  • 1Center for Autoimmunity and Musculoskeletal Diseases, Feinstein Institute for Medical Research , New York, NY , USA.

Frontiers in Immunology
|September 1, 2015
PubMed
Summary

Germinal centers (GCs) are crucial for B cell maturation but can lead to autoimmune diseases like lupus. Defects in GC tolerance mechanisms contribute to the development of pathogenic autoantibodies in systemic lupus erythematosus (SLE).

Keywords:
B cellSLEautoimmunitygerminal centertolerance mechanisms

More Related Videos

Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity
11:12

Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity

Published on: April 11, 2019

7.6K
Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches
09:35

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches

Published on: April 20, 2021

7.4K

Related Experiment Videos

Last Updated: Apr 4, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
12:04

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

Published on: November 1, 2015

19.1K
Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity
11:12

Interrogating Individual Autoreactive Germinal Centers by Photoactivation in a Mixed Chimeric Model of Autoimmunity

Published on: April 11, 2019

7.6K
Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches
09:35

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches

Published on: April 20, 2021

7.4K

Area of Science:

  • Immunology
  • Autoimmunity
  • Molecular Biology

Background:

  • Germinal centers (GCs) are key sites for B cell development, clonal expansion, and affinity maturation.
  • Loss of self-tolerance to autoantigens can occur within GCs during B cell maturation.
  • Systemic lupus erythematosus (SLE) is characterized by a breakdown of tolerance to self-nucleic acid antigens.

Purpose of the Study:

  • To investigate the mechanisms of B cell tolerance breakdown within germinal centers in the context of SLE.
  • To identify specific B cell defects and extrinsic factors contributing to autoantibody production in SLE.

Main Methods:

  • Analysis of B cell populations and their interactions within germinal centers.
  • Examination of genetic factors (e.g., Sle1 locus), signaling pathways (e.g., TLR7), and cellular interactions (e.g., T follicular helper cells).
  • Assessment of apoptotic debris clearance and its impact on B cell tolerance.

Main Results:

  • Pathogenic autoantibodies in SLE can arise from somatic mutation of non-autoreactive B cells within GCs.
  • Multiple factors contribute to GC tolerance loss, including genetic defects, aberrant TLR7 signaling, altered FcRIIB expression, and impaired B cell apoptosis.
  • External factors like Type-1 IFN, BAFF, and increased T follicular helper cells disrupt B cell negative selection.
  • Defective clearance of apoptotic debris promotes autoantibody production via TLR stimulation.

Conclusions:

  • Germinal center B cells are a significant source of autoantibodies in SLE due to defects in tolerance.
  • A complex interplay of intrinsic B cell defects and extrinsic factors drives the loss of GC tolerance in SLE.
  • Targeting GC tolerance mechanisms may offer therapeutic strategies for SLE.