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Leptin promotes SLE by increasing autoantibody production and inhibiting im

Discussion in 'Other Health News and Research' started by Kati, Sep 1, 2016.

  1. Kati

    Kati Patient in training

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    Leptin promotes systemic lupus erythematosus by increasing autoantibody production and inhibiting immune regulation

    http://www.pnas.org/content/early/2016/08/31/1607101113.abstract.html?etoc

    Significance

    Leptin is an adipocytokine whose activity has been associated with the development and maintenance of proinflammatory immune responses. Here we show that genetic deficiency of leptin protected mice from systemic lupus erythematosus (SLE) and reduced production of autoantibodies and renal disease. In a spontaneous animal model of SLE, the administration of leptin promoted an acceleration of the disease, whereas leptin blockade protected from autoimmunity. We suggest that these effects of leptin on SLE could possibly be exploited therapeutically in the disease.

    Abstract

    Leptin is an adipocytokine that plays a key role in the modulation of immune responses and the development and maintenance of inflammation. Circulating levels of leptin are elevated in systemic lupus erythematosus (SLE) patients, but it is not clear whether this association can reflect a direct influence of leptin on the propathogenic events that lead to SLE. To investigate this possibility, we compared the extent of susceptibility to SLE and lupus manifestations between leptin-deficient (ob/ob) and H2-matched leptin-sufficient (wild-type, WT) mice that had been treated with the lupus-inducing agent pristane. Leptin deficiency protected ob/ob mice from the development of autoantibodies and renal disease and increased the frequency of immunoregulatory T cells (Tregs) compared with leptin-sufficient WT mice. The role of leptin in the development of SLE was confirmed in the New Zealand Black (NZB) × New Zealand White (NZW)F1 (NZB/W) mouse model of spontaneous SLE, where elevated leptin levels correlated with disease manifestations and the administration of leptin accelerated development of autoantibodies and renal disease. Conversely, leptin antagonism delayed disease progression and increased survival of severely nephritic NZB/W mice. At the cellular level, leptin promoted effector T-cell responses and facilitated the presentation of self-antigens to T cells, whereas it inhibited the activity of regulatory CD4 T cells. The understanding of the role of leptin in modulating autoimmune responses in SLE can open possibilities of leptin-targeted therapeutic intervention in the disease.


     
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