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T Cell Activation and Clonal Selection

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...

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Optimized Staining and Proliferation Modeling Methods for Cell Division Monitoring using Cell Tracking Dyes

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Single-cell NAD(H) levels predict clonal lymphocyte expansion dynamics.

Lucien Turner¹, Tran Ngoc Van Le¹, Eric Cross^1,2

¹Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.

Science Immunology

|March 15, 2024

Summary

This summary is machine-generated.

Nicotinamide adenine dinucleotide (NAD) biosynthesis controls T cell proliferation by pacing cell cycle entry. Enhancing NAD biosynthesis allows lower-affinity T cells to expand, revealing a metabolic basis for adaptive immunity.

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Area of Science:

Immunology
Metabolic pathways
Cellular dynamics

Background:

Adaptive immunity relies on expanding high-affinity lymphocytes from diverse populations.
Existing models focus on signal transduction, but the role of metabolism is less understood.
Antigen affinity's impact on lymphocyte clonal expansion needs further mechanistic insight.

Purpose of the Study:

To investigate if antigen affinity modulates metabolic pathways to control lymphocyte proliferation.
To identify key metabolic pathways linking T cell receptor affinity to cellular metabolism and expansion.
To explore the role of nicotinamide adenine dinucleotide (NAD) biosynthesis in lymphocyte clonal dynamics.

Main Methods:

Analysis of the T cell receptor affinity-dependent metabolome.
Investigating the role of nicotinamide adenine dinucleotide (NAD) biosynthesis in lymphocyte proliferation.
Single-cell analysis of NAD(H) levels to predict cell division potential in T and B cells.

Main Results:

Nicotinamide adenine dinucleotide (NAD) biosynthesis acts as a central metabolic hub for T cell receptor affinity.
NAD biosynthesis regulates a quiescence exit checkpoint, controlling the pace of lymphocyte proliferation.
Manipulating NAD(H) levels normalized proliferation across affinities and enabled expansion of low-affinity clones; single-cell NAD(H) predicted division potential.

Conclusions:

Antigen affinity tunes metabolic pathways, specifically NAD biosynthesis, to govern lymphocyte clonal expansion.
NAD biosynthesis is a critical metabolic checkpoint controlling lymphocyte proliferation and heterogeneity.
Metabolic pathways are central to controlling single-cell behavior in adaptive immunity.