An IL-2 mutein increases regulatory T cell suppression of dendritic cells via IL-10 and CTLA-4 to promote T cell anergy

Braxton L. Jamison; Matthew Lawrance; Chun Jing Wang; Hannah A. DeBerg; Lauren Ziegler; David M. Sansom; Marc A. Gavin; Lucy S. K. Walker; Daniel Campbell

doi:10.1016/j.celrep.2024.114938

November 1, 2024Cell ReportsOpen Access

An IL-2 mutein increases regulatory T cell suppression of dendritic cells via IL-10 and CTLA-4 to promote T cell anergy

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Key Points

To investigate how an interleukin-2 (IL-2) mutein alters regulatory T cell functionality and suppression of conventional dendritic cells to promote immune tolerance.
Evaluated regulatory T cell functional properties following stimulation with an engineered IL-2 mutein.
Characterized conventional dendritic cell restriction and downstream promotion of T cell anergy mediated by IL-10 and CTLA-4 pathways.
Regulatory T cells show enhanced functional suppressive capacity and direct restriction of conventional dendritic cell activity.
Suppression operates via IL-10 and CTLA-4 pathways to effectively promote antigen-specific T cell anergy for autoimmune disease intervention.

Implication

Experimental study reveals enhanced regulatory T cell suppression of conventional dendritic cells, highlighting therapeutic potential for targeted immunotherapy in autoimmune disease.

Abstract

cells have enhanced functional properties and restrict cDC function, offering promise for targeted immunotherapy use in autoimmune disease.

Discussion

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Cite This Study

Jamison et al. (2024) studied this question.

synapsesocial.com/papers/6a110210d06b5b96589fffb5 https://doi.org/10.1016/j.celrep.2024.114938

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An IL-2 mutein increases regulatory T cell suppression of dendritic cells via IL-10 and CTLA-4 to promote T cell anergy

Key Points

Implication

Abstract

Discussion

Cite This Study

An IL-2 mutein increases regulatory T cell suppression of dendritic cells via IL-10 and CTLA-4 to promote T cell anergy

Key Points

Implication

Abstract

Discussion

Cite This Study

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