FocusAutoimmune Disease

Targeting metabolism for lupus therapy

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Science Translational Medicine  11 Feb 2015:
Vol. 7, Issue 274, pp. 274fs5
DOI: 10.1126/scitranslmed.aaa6731


  • Fig. 1 Many organs, one pathway.

    Shown is a putative mechanism for Met + 2DG–mediated reversal of SLE autoimmunity. SLE is driven by autoreactive CD4+ helper T cells that display increased rates of metabolism through the glycolysis and OXPHOS pathways. Autoreactive T cells promote B-cell activation and autoantibody production (such as antibodies to dsDNA). These antibodies form immune complexes (with antigens) that are deposited in tissues and spur inflammation through a combination of complement activation and innate immune responses. Disease manifestation is dependent on where the inflammation occurs. 2DG and Met block the underlying metabolic defects in autoreactive T cells and potentially innate immune cells as well, reducing inflammation associated with SLE.


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