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    Obesity-Induced Metabolic Stress Leads to Biased Effector Memory CD4+ T Cell Differentiation via PI3K p110d-Akt-Mediated Signals

    Access Status
    Open access via publisher
    Authors
    Mauro, C.
    Smith, J.
    Cucchi, D.
    Coe, D.
    Fu, H.
    Bonacina, F.
    Baragetti, A.
    Cermenati, G.
    Caruso, D.
    Mitro, N.
    Catapano, A.
    Ammirati, E.
    Longhi, M.
    Okkenhaug, K.
    Norata, Giuseppe
    Marelli-Berg, F.
    Date
    2017
    Type
    Journal Article
    
    Metadata
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    Citation
    Mauro, C. and Smith, J. and Cucchi, D. and Coe, D. and Fu, H. and Bonacina, F. and Baragetti, A. et al. 2017. Obesity-Induced Metabolic Stress Leads to Biased Effector Memory CD4+ T Cell Differentiation via PI3K p110d-Akt-Mediated Signals. Cell Metabolism. 25 (3): pp. 593-609.
    Source Title
    Cell Metabolism
    DOI
    10.1016/j.cmet.2017.01.008
    ISSN
    1550-4131
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/55371
    Collection
    • Curtin Research Publications
    Abstract

    © 2017 The Author(s) Low-grade systemic inflammation associated to obesity leads to cardiovascular complications, caused partly by infiltration of adipose and vascular tissue by effector T cells. The signals leading to T cell differentiation and tissue infiltration during obesity are poorly understood. We tested whether saturated fatty acid-induced metabolic stress affects differentiation and trafficking patterns of CD4 + T cells. Memory CD4 + T cells primed in high-fat diet-fed donors preferentially migrated to non-lymphoid, inflammatory sites, independent of the metabolic status of the hosts. This was due to biased CD4 + T cell differentiation into CD44 hi -CCR7 lo -CD62L lo -CXCR3 + -LFA1 + effector memory-like T cells upon priming in high-fat diet-fed animals. Similar phenotype was observed in obese subjects in a cohort of free-living people. This developmental bias was independent of any crosstalk between CD4 + T cells and dendritic cells and was mediated via direct exposure of CD4 + T cells to palmitate, leading to increased activation of a PI3K p110d-Akt-dependent pathway upon priming.

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