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Related Concept Videos

T Cell Activation and Clonal Selection01:22

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.
Naive T cells that have not yet encountered an antigen express two primary CD...
T Cell Types and Functions01:24

T Cell Types and Functions

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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TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...

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Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses
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CD8-β ADP-ribosylation affects CD8(+) T-cell function.

Timo Lischke1, Valéa Schumacher, Janusz Wesolowski

  • 1Institute of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. t.lischke@uke.de

European Journal of Immunology
|April 12, 2013
PubMed
Summary

Extracellular NAD(+) causes ADP-ribosylation of the CD8-β molecule on CD8(+) T cells via ART2.2, impairing their ability to recognize peptide:MHC-I complexes and reducing T-cell cytotoxicity.

Keywords:
AntibodiesCell surface moleculesT cellsTransgenic/knockout mice

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Area of Science:

  • Immunology
  • Molecular Biology
  • Biochemistry

Background:

  • The CD8αβ coreceptor is essential for CD8(+) T cell recognition of peptide:MHC-I complexes.
  • Adenosine diphosphate ribosyl transferase 2.2 (ART2.2) modifies extracellular proteins using NAD(+) and ADP-ribose.

Purpose of the Study:

  • To investigate the effect of extracellular NAD(+) on CD8β modification and function.
  • To determine the role of ART2.2 in NAD(+)-induced CD8β modification.

Main Methods:

  • In vitro and in vivo experiments using murine CD8(+) T cells.
  • Antibody epitope mapping and tetramer binding assays.
  • Assessment of T-cell cytotoxicity in wild-type and ART2-deficient mice.

Main Results:

  • NAD(+) treatment led to ADP-ribosylation of CD8-β on T cells, dependent on ART2.2.
  • This modification altered specific epitopes on CD8-β, affecting antibody binding.
  • NAD(+)-treated CD8(+) T cells showed impaired binding to MHC-I tetramers and reduced cytotoxic activity in vivo.

Conclusions:

  • ADP-ribosylation of CD8-β by ART2.2 in the presence of NAD(+) can regulate CD8 coreceptor function.
  • This mechanism may play a role in modulating T-cell responses under conditions of elevated extracellular NAD(+).