26rhk031
10.3205/26rhk031
urn:nbn:de:0183-26rhk0316
Meeting Abstract
FATP2 is the receptor for fatty acids on CD4 +T cells in JIA at the site of inflammation
Subramanyam
Subramanyam
Sudheendra Hebbar
SH
RWTH University Hospital, Aachen, Deutschland
author
Ohl
Ohl
Kim
K
Hochschule Niederrhein, Mönchengladbach, Deutschland
RWTH University Hospital, Aachen, Deutschland
author
Rajendiran
Rajendiran
Anandhi
A
RWTH University Hospital, Aachen, Deutschland
author
Hriczko
Hriczko
Judit Turyne
JT
RWTH University Hospital, Aachen, Deutschland
author
de Jong
de Jong
Renske
R
RWTH University Hospital, Aachen, Deutschland
author
Neullens
Neullens
Christopher
C
RWTH University Hospital, Aachen, Deutschland
author
Mashregi
Mashregi
Mir Farzin
MF
DRFZ, Berlin, Deutschland
author
van Loosdregt
van Loosdregt
Jorg
J
UMC, Utrecht, Niederlande
author
Vastert
Vastert
Bas
B
UMC, Utrecht, Niederlande
author
Tenbrock
Tenbrock
Klaus
K
Inselpital Bern University Hospital, Bern, Schweiz
RWTH University Hospital, Aachen, Deutschland
author
German Medical Science GMS Publishing House
Düsseldorf
610
20260909
engl
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung).
M0656
031
Deutsche Gesellschaft für Rheumatologie
Deutsche Gesellschaft für Orthopädische Rheumatologie
Gesellschaft für Kinder- und Jugendrheumatologie
54. Kongress der Deutschen Gesellschaft für Rheumatologie und Klinische Immunologie (DGRh), 36. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR), 40. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh)
Deutscher Rheumatologiekongress 2026
Experimentelle & Translationale Rheumatologie
Leipzig
20260909
20260912
ET.03
TextIntroduction: Juvenile idiopathic arthritis (JIA) is a chronic inflammatory joint disorder affecting children, in which T cells function within a microenvironment characterized by low glucose and elevated fatty acid levels. The metabolic mechanisms that allow T cells to adapt and remain active under these nutrient-limited conditions are still not well understood.Methods: We examined T cells from both the peripheral blood (PB) and Synovial fluid (SF) of JIA patients and conducted bulk gene expression analysis and single-cell RNA sequencing. These analyses revealed increased expression of Fatty Acid Transport Protein 2 (FATP2), which was confirmed by flow cytometry. We then investigated the effects of inhibiting FATP2 using the compound lipofermata in vitro through flow cytometry and RNA sequencing and in vivo using a collagen-induced arthritis mouse model.Results: T cells from SF showed significantly higher fatty acid uptake and FATP2 expression compared to PB T cells, particularly in activated and memory T cell subsets. Inhibition of FATP2 with lipofermata reduced fatty acid uptake, T cell proliferation, and interferon-γ production through pAKT3/mTOR-dependent pathway. However, lipofermata treatment did not alleviate arthritis symptoms in mice, likely because FATP2 is not similarly regulated in mouse memory T cells. Analysis of open-source sequencing data indicates FATP2 is also upregulated in psoriatic and rheumatoid arthritis at sites of inflammation. A humanized psoriatic arthritis mouse model is planned.Conclusion: These findings indicate that T cells in JIA adapt to a fatty acid–rich environment by increasing FATP2 expression. Disrupting this metabolic adaptation through FATP2 inhibition may represent a potential therapeutic strategy for treating JIA and other autoimmune inflammatory diseases.
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