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@ARTICLE{Kraus:212548,
      author       = {F. V. Kraus and S. Keck and K. Klika$^*$ and J. Graf and R.
                      A. Carvalho and H.-M. Lorenz and M. M. Souto-Carneiro},
      title        = {{R}eduction of pro-inflammatory effector functions through
                      remodeling of fatty acid metabolism in {CD}8+ {T}-cells from
                      rheumatoid arthritis patients.},
      journal      = {Arthritis $\&$ rheumatology},
      volume       = {75},
      number       = {7},
      issn         = {2326-5191},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DKFZ-2023-00233},
      pages        = {1098-1109},
      year         = {2023},
      note         = {2023 Jul;75(7):1098-1109},
      abstract     = {Rheumatoid arthritis (RA) CD8+ T-cells (CD8) maintain their
                      effector pro-inflammatory phenotype by changing their
                      metabolism towards aerobic glycolysis. However, their
                      massive energetic and biosynthetic needs may require
                      additional substrates other than glucose. Since systemic
                      alterations in lipid metabolism have been reported in RA
                      patients, we explored the role of fatty acid (FA) metabolism
                      in CD8 to identify potential targets to curb their
                      pro-inflammatory potential.The expression of FA
                      metabolism-related genes was analyzed for total and
                      CD8-subsets in the data of RA patients and healthy controls
                      retrieved from the gene expression omnibus database.
                      Functional assays were performed on peripheral-blood CD8
                      isolated from RA (n=31), PsA (n=26), and SpA (n=21) patients
                      under different therapies (DMARD, biologicals, and JAK
                      inhibitors) and controls (n=13). We quantified the
                      expression of FA transporters, lipid uptake, intracellular
                      FA content, cytokine production, activation, proliferation,
                      and capacity to inhibit tumor cell growth, either with or
                      without FA metabolism inhibitors.The CD8 gene expression
                      profile of FA metabolism-related genes was significantly
                      different between untreated RA patients and controls. RA
                      patients with a good clinical response after 6 months MTX
                      therapy significantly increased the expression of FA
                      metabolism-related genes. Cell-surface expression of FA
                      transporters FABP4 and GPR84 and FA uptake was higher in
                      effector and memory CD8 of RA patients than for controls. In
                      vitro blockade of FA metabolism significantly impaired CD8
                      effector functions.RA CD8 present an altered FA metabolism
                      which can provide potential therapeutic targets to control
                      the pro-inflammatory profile. Particularly, therapies
                      directed against the transport and oxidation of free FA.},
      cin          = {W160},
      ddc          = {610},
      cid          = {I:(DE-He78)W160-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36704915},
      doi          = {10.1002/art.42456},
      url          = {https://inrepo02.dkfz.de/record/212548},
}