Re-evaluating “autoimmunity” to account for persistent infection:
I’ve published several papers on persistent infection + microbiome dysbiosis as drivers of “autoimmune” disease. So I was glad that many 2018 papers added to a growing body of research documenting “autoantibody” production in response to a range of bacterial, viral and fungal pathogens (as opposed to “self”). These pathogens are not short-term “triggers” but persist as members of complex microbiome communities. These are two of my favorite 2018 studies on the topic:
Lead author: Martin Kriegel, Yale School of Medicine
The team detected Enterococcus galinarum (a common human gut bacteria) in the mesenteric veins, lymph nodes, spleens and livers of mice made genetically prone to autoimmunity. In these mice, the bacterium initiated the production of “autoantibodies,” inflammation and activated T cells. However, this “autoantibody” production stopped when E. gallinarum’s growth was suppressed with the antibiotic vancomycin or with an intramuscular vaccine. In addition, E. gallinarum–specific DNA was recovered from liver biopsies of human autoimmune patients, and co-cultures with human liver cells replicated the mouse findings.
Lead author: Manuel Rodriguez, Mayo Clinic and Foundation
The team studied CD4+ T cells from the cerebrospinal fluid of patients with multiple sclerosis. They found that these T cells (which are capable of inducing an inflammatory response associated w/ demyelination) could be activated by an enzyme created by bacteria frequently found in the gut microbiome of MS patients.
Paper highlight: “These tantalizing results [in multiple sclerosis] identify a new autoantigen and suggest that one possible trigger of disease could be cross-reactivity to microbiota-derived peptides”