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Updated: May 9, 2026

08:59
T and B Cell Receptor Immune Repertoire Analysis using Next-generation Sequencing
Published on: January 12, 2021
T Cell Plasticity in Systemic Lupus Erythematosus Revealed by Large-Scale T Cell Receptor Repertoire and
Yasuo Nagafuchi1,2,3,4, Masahiro Nakano3, Kaitlyn A Lagattuta5,6,7,8,9
1Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Arthritis & Rheumatology (Hoboken, N.J.)
|May 8, 2026
Summary
In systemic lupus erythematosus (SLE), CD4+ T cells show plasticity. Specifically, effector regulatory T cells (eTregs) can transform into Th1 cells, a process linked to disease activity.
Area of Science:
- Immunology
- T cell biology
- Autoimmune diseases
Background:
- CD4+ T cell plasticity is crucial in immune responses.
- Understanding T cell plasticity in systemic lupus erythematosus (SLE) is vital for disease management.
- T cell receptor (TCR) repertoire analysis offers insights into T cell lineage history.
Purpose of the Study:
- To characterize CD4+ T cell plasticity in human SLE.
- To use TCR repertoire features and transcriptomics to identify plasticity patterns.
- To assess the association between T cell plasticity and SLE clinical disease activity.
Main Methods:
- Utilized TCR repertoire data and transcriptomic profiling from the ImmuNexUT database (117 SLE cases).
- Quantified T cell plasticity across 13 T cell types using 6,392 samples.
- Defined cell-type and disease signatures, evaluated plasticity via signature correlations and TCR clonotype overlap, with independent cohort replication.
Main Results:
- Identified orthogonal repertoire and transcriptome signatures, revealing comprehensive CD4+ T cell plasticity.
- Observed significant plasticity between effector regulatory T cells (eTregs) and Th1 cells, replicated in an independent cohort.
- SLE Th1 cells displayed Treg-like TCR features and transcriptomic profiles; Th1 'Tregness' correlated positively with SLE disease activity.
Conclusions:
- Identified a Treg-associated Th1 cell state in human SLE.
- Findings support Treg-to-Th1 plasticity as a mechanism in SLE pathogenesis.
- This plasticity is linked to SLE disease activity, suggesting potential therapeutic targets.
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