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Commensal microbiota influence systemic autoimmune responses.

Jens T Van Praet1, Erin Donovan1, Inge Vanassche1

  • 1Laboratory for Molecular Immunology and Inflammation, Department of Rheumatology, Ghent University Hospital, Ghent, Belgium.

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|January 21, 2015
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Summary
This summary is machine-generated.

Neonatal gut microbiota colonization, particularly segmented filamentous bacteria, can trigger autoimmune responses and antinuclear antibody production in mice lacking key immune organs. This suggests early-life gut bacteria influence adult generalized autoimmunity.

Keywords:
antinuclear antibodiescommensal microbiotasystemic autoimmunity

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Area of Science:

  • Immunology
  • Microbiology
  • Autoimmunity

Background:

  • Antinuclear antibodies (ANAs) are key indicators of autoimmune diseases like lupus and scleroderma.
  • The mechanisms driving loss of self-tolerance to nuclear components are not fully understood.

Purpose of the Study:

  • To investigate the origins of spontaneous antinuclear antibody development in mice lacking secondary lymphoid organs.
  • To explore the role of gut microbiota and immune signaling in the development of systemic autoimmunity.

Main Methods:

  • Utilized genetically modified mice deficient in lymphotoxin and Hox11.
  • Performed cell-specific deletion and in vivo lymphotoxin blockade.
  • Assessed the impact of commensal gut flora, including segmented filamentous bacteria, and IL-17 receptor signaling.

Main Results:

  • Mice lacking secondary lymphoid organs spontaneously developed antinuclear antibodies.
  • This autoimmune phenotype was not due to central tolerance defects.
  • Autoimmunity was linked to neonatal gut-associated lymphoid tissue formation and influenced by gut microbiota and IL-17 signaling.

Conclusions:

  • Neonatal gut microbiota colonization plays a critical role in the development of generalized autoimmunity in adult life.
  • Specific gut bacteria and associated immune signaling pathways can promote the production of antinuclear antibodies.