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Limiting IgA productionAdd to my bookmarks

Nature Immunology

October 1, 2012

How the body limits the amount of circulating IgA antibody in the blood on mice, and thereby lowering the risk of kidney disease is described in a paper published online this week in Nature Immunology. The findings could help with therapeutic intervention for those afflicted with IgA-mediated autoimmunity.

Shao-Cong Sun and colleagues studied B immune cells, which are the body’s antibody-producing cells. Activation of these B cells ramps up antibody production and can induce a process known as immunoglobulin class switching, a genetic process that dictates the type of antibody that is eventually produced. Sun’s study shows a regulatory molecule called TBK1 specifically prevents class switching to IgA. Mice that lacked TBK1 expression in B cells produced higher amounts of IgA in their serum, including autoantibodies that recognize self-tissues. These mice developed renal dysfunction as autoimmune IgA complexes accumulated in their kidneys, mimicking IgA-related human pathologies.

DOI:10.1038/ni.2423 | Original article

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