In the new study, described in an online Early Edition of the Proceedings of the National Academy of Sciences the week of February 4, 2013, the researchers determined that the absence of a certain type of immune cell, or of a key signaling molecule within the cell, greatly reduces the development of autoimmunity in mouse models of lupus. Mice with these protective changes showed little impairment of their normal immune functions.
The cycle apparently begins when certain immune cells mistakenly detect self-proteins and nucleic acids as “foreign” and begin pumping out type I interferons. This mobilizes other elements of the immune system, including the antibody response, and soon autoantibodies are attacking self-molecules in healthy cells. The autoantibodies in turn present these “foreign” molecules to type I interferon-producing cells, adding fuel to the autoimmune fire.
Mika Ono | EurekAlert!
Further reports about: > Drug Delivery > Immunology > Lupus erythematodes > Microbial Nitrogen > Nobel Prize > SLC15A4 > Scripps > Theofilopoulos > blood clot > cellular protein > dendritic cells > health services > healthy cell > immune cell > immune system > immunosuppressive drug > inflammatory disease > mouse model > mutant mice > nucleic acids > rheumatoid arthritis > signaling pathway > type I interferon > viral infection
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