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The microbiome in SLE pathogenesis

Systemic lupus erythematosus (SLE), the embodiment of a multi-organ autoimmune disease, results from hyperactivation of host-defence pathways and immune recognition of the most fundamental building blocks of life. In 2018, key advances have placed intestinal immunity and dysregulated expansions of candidate pathobionts at the forefront of SLE pathogenesis.

Key advances

  • Pathobiont translocation from the small intestine to the liver in lupus-prone mice, and in a subset of patients with systemic lupus erythematosus (SLE), might drive the expression of interferon-related genes and autoantibody production2.

  • Immune priming to primitive bacterial commensal orthologues of the ribonucleoprotein Ro60 results in both physiological autoimmunity and disease-associated autoimmunity in predisposed individuals4.

  • Patients with SLE had a restricted gut microbiota diversity of similar composition to patients with Sjögren syndrome; by contrast, the oral microbiota composition of these two patient groups differed substantially7.

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Fig. 1: Potential pathobiont mechanisms that contribute to SLE pathogenesis.


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The author declares that he is supported by grants from the NIH and the Judith and Stewart Colton Autoimmunity Center.

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Correspondence to Gregg J. Silverman.

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Silverman, G.J. The microbiome in SLE pathogenesis. Nat Rev Rheumatol 15, 72–74 (2019).

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