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An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

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Homocitrullinated Peptides Drive Pro-Inflammatory T Cell Responses in a Humanized Mouse Model of Rheumatoid

Sofya Ulanova¹, Jaspreet Kaur¹, Gabrielle Buckley¹

¹Department of Microbiology & Immunology, Western University, London, Ontario, Canada.

Arthritis & Rheumatology (Hoboken, N.J.)

|June 8, 2026

Summary

Anti-homocitrullinated peptide (HomoCitP) responses in rheumatoid arthritis (RA) were studied. HomoCitP induced T-cell activation and exhaustion, suggesting a role in RA pathogenesis and potential therapeutic targets.

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Published on: January 31, 2020

Area of Science:

Immunology
Rheumatology
Autoimmunity

Background:

Anti-homocitrullinated protein/peptide antibodies are specific to rheumatoid arthritis (RA).
T-cell responses to homocitrullinated peptides (HomoCitP) are largely unexplored.
The strongest genetic risk factor for RA is the human leukocyte antigen (HLA)-DR4 gene.

Purpose of the Study:

To investigate T-cell responses to HomoCitP in a humanized HLA-DR4-transgenic (DR4tg) mouse model of RA.
To explore the pathogenic role of autoreactivity to HomoCitP in RA.

Main Methods:

DR4tg mice were immunized with a HomoCitP (HomoCitJED) or control.
T-cells from draining lymph nodes and spleens were analyzed for phenotype, cytokine production, and proliferation.
Flow cytometry, ELISAs, and ProQuantum™ immunoassays were utilized.

Main Results:

HomoCitJED immunization induced robust expansion of Th1, Th17, and Th1/Th17 cells.
Effector activity was confirmed by increased IL-17A, TNF-α, and IFN-γ production.
Both CD4+ and CD8+ T cells showed increased activation and exhaustion markers, alongside augmented proliferation.

Conclusions:

HomoCitP elicits dysregulated Th1/Th17 and Tc1/Tc17 responses.
Imbalance in homocitrulline-driven CD4+ and CD8+ T-cells may contribute to RA pathogenesis.
These T-cell responses represent potential targets for immunomodulatory therapies in RA.