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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.
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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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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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Related Experiment Video

Updated: Feb 20, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
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Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

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Altered B-cell signaling in lupus.

Kui Liu1, Chandra Mohan

  • 1Division of Rheumatology, and Center for Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390-8884, USA. Kui.Liu@utsouthwestern.edu

Autoimmunity Reviews
|August 30, 2008
PubMed
Summary

Systemic lupus erythematosus (SLE) involves autoantibodies and end-organ damage. Studying B-cell signaling in lupus models offers insights into autoimmune B-cell survival and potential therapeutic strategies for SLE.

Area of Science:

  • Immunology
  • Autoimmunity
  • Molecular Biology

Background:

  • Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by autoantibodies and organ damage.
  • Aberrant lymphocyte signaling is implicated in SLE pathogenesis and represents a therapeutic target.
  • Murine models of lupus offer valuable insights into lymphocyte signaling alterations seen in human patients.

Purpose of the Study:

  • To investigate B-cell signaling pathways in murine models of lupus.
  • To understand the mechanisms underlying the enhanced survival of autoreactive B cells in lupus.
  • To identify potential therapeutic targets for SLE based on B-cell signaling.

Main Methods:

  • Analysis of B-cell signaling in various conventional and engineered murine lupus models.

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  • Comparison of signaling alterations in murine lupus models with patient samples.
  • In-depth examination of signaling pathways critical for B-cell survival.

    • Main Results:

    • Murine lupus models recapitulate key B-cell signaling abnormalities observed in SLE patients.
    • Specific signaling events contributing to autoreactive B-cell survival were elucidated.
    • These findings provide a deeper understanding of lupus pathogenesis.

    Conclusions:

    • B-cell signaling analysis in lupus models is crucial for understanding SLE.
    • Targeting aberrant B-cell signaling pathways presents a promising therapeutic avenue for SLE.
    • Further research into these pathways could lead to novel treatments for lupus patients.