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Related Concept Videos

Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...
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T Cell Activation and Clonal Selection

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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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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The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
Phagocytes
Phagocytes police the peripheral tissues by removing cellular debris and responding to the invasion of foreign substances or pathogens. Many phagocytes attack and remove microorganisms even before lymphocytes detect them. The human body has two general...
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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...

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Related Experiment Video

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A Colorimetric Assay that Specifically Measures Granzyme B Proteolytic Activity: Hydrolysis of Boc-Ala-Ala-Asp-S-Bzl
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Bcl6 controls granzyme B expression in effector CD8+ T cells.

Kazuki Yoshida1, Akemi Sakamoto, Kimihiro Yamashita

  • 1Department of Developmental Genetics, Graduate School of Medicine, Chiba University, Chiba, Japan.

European Journal of Immunology
|November 28, 2006
PubMed
Summary

Bcl6 (B-cell lymphoma 6) represses granzyme B in effector CD8(+) T cells, reducing their killing activity. This study identifies granzyme B as a direct molecular target of Bcl6 in these crucial immune cells.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Cellular Biology

Background:

  • Bcl6 (B-cell lymphoma 6) is crucial for memory CD8(+) T cell development and maintenance.
  • The function of Bcl6 in effector CD8(+) T cells remains largely uncharacterized.
  • Effector CD8(+) T cells are essential for eliminating infected or cancerous cells.

Purpose of the Study:

  • To investigate the role of Bcl6 in effector CD8(+) T cells.
  • To determine if Bcl6 directly regulates effector molecules in CD8(+) T cells.
  • To elucidate the molecular mechanisms by which Bcl6 influences CD8(+) T cell function.

Main Methods:

  • Analysis of Bcl6 expression in activated and effector CD8(+) T cells.
  • Correlation analysis between Bcl6 mRNA and granzyme B mRNA levels.
  • Overexpression studies of Bcl6 in CD8(+) T cells to assess killing activity.
  • Chromatin immunoprecipitation (ChIP) assays to detect Bcl6 binding to the granzyme B promoter.
  • Luciferase reporter assays to confirm Bcl6-mediated repression of granzyme B transcription.

Main Results:

  • Bcl6 expression is transiently induced upon CD8(+) T cell activation and continuously upregulated in effector cells.
  • Higher Bcl6 mRNA levels inversely correlate with granzyme B mRNA levels in effector CD8(+) T cells.
  • Overexpression of Bcl6 diminishes the cytotoxic activity of effector CD8(+) T cells by reducing granzyme B expression.
  • A specific Bcl6-binding DNA sequence was identified in the granzyme B promoter.
  • Bcl6 binds to this sequence in naive CD8(+) T cells, but binding is lost upon activation.
  • This binding sequence is essential for Bcl6 to repress granzyme B gene expression.

Conclusions:

  • Bcl6 acts as a transcriptional repressor of granzyme B in effector CD8(+) T cells.
  • The granzyme B gene is a direct molecular target of Bcl6 in the context of effector CD8(+) T cell function.
  • Bcl6-mediated repression of granzyme B contributes to the regulation of CD8(+) T cell cytotoxicity during the effector phase.