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Related Concept Videos

B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

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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...
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Defense Against Bacterial Pathogens01:31

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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
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T Cell Activation and Clonal Selection01:22

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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.
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Special Features of Adaptive Immunity01:20

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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.
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Diversity of Antigen Receptors01:28

Diversity of Antigen Receptors

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Antigen receptors are essential components of the immune system crucial in defending the body against foreign invaders. These receptors are present on the surface of B and T cells, enabling them to recognize antigens and mount an appropriate immune response.
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T Cell Types and Functions01:24

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Related Experiment Video

Updated: Sep 20, 2025

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
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For whom the B cells toll.

Elissa K Deenick1,2, Alisa Kane1,3,4,5

  • 1Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.

Immunology and Cell Biology
|June 7, 2022
PubMed
Summary

Researchers discovered a new genetic cause of systemic lupus erythematosus (SLE). This autoimmune disease results from specific gene mutations that overactivate Toll-like receptor 7 (TLR7) signaling pathways.

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Area of Science:

  • Immunology
  • Genetics
  • Rheumatology

Background:

  • Systemic lupus erythematosus (SLE) is a complex autoimmune disease with diverse clinical manifestations.
  • The precise genetic underpinnings of many SLE cases remain incompletely understood.
  • Toll-like receptor 7 (TLR7) plays a crucial role in innate immunity and has been implicated in SLE pathogenesis.

Purpose of the Study:

  • To identify novel genetic factors contributing to the development of systemic lupus erythematosus.
  • To elucidate the molecular mechanisms linking specific genetic mutations to aberrant immune responses in SLE.
  • To investigate the role of Toll-like receptor 7 (TLR7) signaling in a newly identified monogenic form of SLE.

Main Methods:

  • Genetic sequencing to identify mutations in affected individuals.
  • In vitro assays to assess the functional impact of identified mutations on TLR7 signaling.
  • Analysis of immune cell activation and cytokine production in response to TLR7 stimulation.

Main Results:

  • Identification of a novel monogenic form of SLE.
  • Specific mutations were found to cause constitutive and/or enhanced signaling through Toll-like receptor 7 (TLR7).
  • Increased TLR7 signaling leads to heightened type I interferon production and downstream autoimmune responses.

Conclusions:

  • Mutations leading to increased Toll-like receptor 7 (TLR7) signaling represent a distinct monogenic cause of systemic lupus erythematosus.
  • Targeting TLR7 signaling pathways may offer a potential therapeutic strategy for this specific SLE subgroup.
  • This finding expands our understanding of the genetic heterogeneity and immunopathogenesis of SLE.