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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

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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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B Cell Activation and Differentiation01:24

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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.
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Related Experiment Video

Updated: May 23, 2025

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
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IL-4 alters TLR7-induced B cell developmental program in lupus.

Changming Lu1, Shanrun Liu1, Min Gao2

  • 1Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

Clinical Immunology (Orlando, Fla.)
|March 11, 2025
PubMed
Summary
This summary is machine-generated.

Interleukin-4 (IL-4) therapy reduces autoantibodies in systemic lupus erythematosus (SLE) by reprogramming B cell development. This therapy counteracts Toll-like receptor 7 (TLR7)-driven B cell populations implicated in SLE pathogenesis.

Keywords:
B cell(2)IL-4(3)TLR7(4)autoantibodies(6)lupus(1)transcriptomics(5)

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Area of Science:

  • Immunology
  • Autoimmunity
  • B cell biology

Background:

  • Toll-like receptor 7 (TLR7) stimulation drives autoantibody production in systemic lupus erythematosus (SLE) via specific B cell subsets.
  • Double-negative 2 (DN2) B cells, characterized as T-bet+CD11c+IgD-CD27-, are key players in this pathogenic process.

Purpose of the Study:

  • To investigate the therapeutic potential of Interleukin-4 (IL-4) in modulating TLR7-induced B cell responses in SLE.
  • To determine how IL-4 affects the development and phenotype of B cells in the context of TLR7 activation.

Main Methods:

  • Administration of IL-4 to autoimmune BXD2 mice treated with the TLR7 agonist R848.
  • Single-cell transcriptomics analysis to assess B cell populations and gene expression.
  • In vitro stimulation of SLE patient B cells with a DN2 polarizing cocktail and IL-4.

Main Results:

  • IL-4 treatment significantly reduced autoantibodies and pathogenic T-bet+CD11c+IgD- B cells in mice.
  • IL-4 redirected B cell development towards follicular, CD23+ germinal center (GC), and DN4-like memory B cells.
  • IL-4 suppressed R848-induced GC B cell proliferation and reduced interferon response genes in SLE patient B cells.

Conclusions:

  • IL-4 administration effectively counteracts TLR7-driven DN2 and GC B cell populations in SLE models.
  • IL-4 promotes a developmental reprogramming of B cells, offering a potential therapeutic strategy for SLE.