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PreprintCC BYbioRxiv

A Single-Cell Framework for Classifying Human Th17 Pathogenicity Links Acylcarnitine Metabolism to Non-Pathogenic Inflammation in Type 2 Diabetes

  • N. S. Ujagar
  • S. Poudel
  • S. Saraswat
  • S. Sureshchandra
  • J. Kim
  • U.-V. Le
  • A. R. Jones
  • N. Hopkins
  • T. Sriram
  • M. Matson
  • E. H. Pilier
  • M. Mejia
10 more authors
  • S. S. Bailin
  • C. N. Wanjalla
  • M. Y. Sy
  • D. C. Newcomb
  • C. Walsh
  • L. E. Wagar
  • B. S. Nikolajczyk
  • X. D. Zhang
  • D. R. Green
  • D. A. Nicholas1
  1. 1University of California, Irvine
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Abstract

Th17 cells are categorized as non-pathogenic (Th17np) and pathogenic (Th17p), states defined primarily in murine autoimmune models. In contrast, studying these states in humans remains difficult because these subsets lack validated identifiers. We developed a nanovial-based single-cell ELISA to isolate cytokine-secreting human Th17 cells and define Th17np vs Th17p cell transcriptional states. These signatures enabled predictive classification and flow-cytometric identification across tissues and diseases. Application of these strategies with single-cell metabolic modeling and functional profiling revealed that Th17np cells predominate in type 2 diabetes yet exhibit impaired fatty acid oxidation capacity despite elevated carnitine palmitoyltransferase 1A (CPT1A). CRISPR perturbation and pharmacologic inhibition identified acylcarnitine metabolism as a regulator of Th17 state balance and exposed a selective metabolic vulnerability in type 2 diabetes. This framework links human Th17 cell pathogenicity to lipid metabolism.

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Cite

BibTeXRIS
BibTeX
@misc{ujagar2026singlecell,
  title = {{A Single-Cell Framework for Classifying Human Th17 Pathogenicity Links Acylcarnitine Metabolism to Non-Pathogenic Inflammation in Type 2 Diabetes}},
  author = {N. S. Ujagar and S. Poudel and S. Saraswat and S. Sureshchandra and J. Kim and U.-V. Le and A. R. Jones and N. Hopkins and T. Sriram and M. Matson and E. H. Pilier and M. Mejia and S. S. Bailin and C. N. Wanjalla and M. Y. Sy and D. C. Newcomb and C. Walsh and L. E. Wagar and B. S. Nikolajczyk and X. D. Zhang and D. R. Green and D. A. Nicholas},
  howpublished = {bioRxiv},
  year = {2026},
  month = sep,
  doi = {10.64898/2026.09.01.748572},
  url = {https://www.biorxiv.org/content/10.64898/2026.09.01.748572v1},
  note = {CC BY},
}
RIS
TY  - UNPB
TI  - A Single-Cell Framework for Classifying Human Th17 Pathogenicity Links Acylcarnitine Metabolism to Non-Pathogenic Inflammation in Type 2 Diabetes
AU  - N. S. Ujagar
AU  - S. Poudel
AU  - S. Saraswat
AU  - S. Sureshchandra
AU  - J. Kim
AU  - U.-V. Le
AU  - A. R. Jones
AU  - N. Hopkins
AU  - T. Sriram
AU  - M. Matson
AU  - E. H. Pilier
AU  - M. Mejia
AU  - S. S. Bailin
AU  - C. N. Wanjalla
AU  - M. Y. Sy
AU  - D. C. Newcomb
AU  - C. Walsh
AU  - L. E. Wagar
AU  - B. S. Nikolajczyk
AU  - X. D. Zhang
AU  - D. R. Green
AU  - D. A. Nicholas
PY  - 2026
DA  - 2026/09/01
PB  - bioRxiv
DO  - 10.64898/2026.09.01.748572
UR  - https://www.biorxiv.org/content/10.64898/2026.09.01.748572v1
AB  - Th17 cells are categorized as non-pathogenic (Th17np) and pathogenic (Th17p), states defined primarily in murine autoimmune models. In contrast, studying these states in humans remains difficult because these subsets lack validated identifiers. We developed a nanovial-based single-cell ELISA to isolate cytokine-secreting human Th17 cells and define Th17np vs Th17p cell transcriptional states. These signatures enabled predictive classification and flow-cytometric identification across tissues and diseases. Application of these strategies with single-cell metabolic modeling and functional profiling revealed that Th17np cells predominate in type 2 diabetes yet exhibit impaired fatty acid oxidation capacity despite elevated carnitine palmitoyltransferase 1A (CPT1A). CRISPR perturbation and pharmacologic inhibition identified acylcarnitine metabolism as a regulator of Th17 state balance and exposed a selective metabolic vulnerability in type 2 diabetes. This framework links human Th17 cell pathogenicity to lipid metabolism.
ER  -