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Study Offers Clues To Origins Of Autoimmunity

Date:
October 3, 2005
Source:
National Jewish Medical and Research Center
Summary:
Researchers at National Jewish Medical and Research Center have discovered a mechanism in the body that could lead to autoimmune diseases, such as lupus, rheumatoid arthritis, or diabetes. The research team, led by John Cambier, Ph.D., found that potentially harmful B cells circulating in the body are not permanently silenced as previously thought; they can awaken and regain the ability to launch an attack against the body's own tissue.
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Researchers at National Jewish Medical and Research Centerhave discovered a mechanism in the body that could lead to autoimmunediseases, such as lupus, rheumatoid arthritis, or diabetes. Theresearch team, led by John Cambier, Ph.D., found that potentiallyharmful B cells circulating in the body are not permanently silenced aspreviously thought; they can awaken and regain the ability to launch anattack against the body's own tissue. The findings were publishedonline October 2 by Nature Immunology.

"Keeping self-reactive Bcells in a quiescent state is crucial for the prevention ofautoimmunity," said Dr. Cambier, Professor and Chairman of theIntegrated Department of Immunology at National Jewish and theUniversity of Colorado Health Sciences Center. "Our findings show howthese cells can be reactivated and suggest lines of research that maylead to therapies for autoimmune diseases."

B cells are part ofthe immune system. When properly stimulated, they produce antibodies,which bind to foreign molecules and neutralize them or target the cellsthey are part of for destruction. The body, in its attempt to protectagainst any foreign invader, produces a huge variety of B cells, eachcapable of recognizing a different molecule, also called an antigen.

However,in the course of generating such a variety of B cells, the immunesystem also produces ones that recognize normal components of the bodyas antigens. Were those cells to become activated, they would initiatean attack against the body's own tissue. Fortunately, these cells aresent into a sort of suspended animation, known as anergy, when theyencounter the antigen but fail to receive additional signals necessaryto activate their antibody-producing machinery.

For years,scientists have thought that one encounter with an antigen would send aB cell into permanent anergy. Dr. Cambier and his colleagues showed,however, that self-reactive B cells need constant stimulation by theirantigen to remain anergic, and that removing the antigen allows them toregain their normal, ready state.

The researchers suggest that anactive infection could draw a self-reactive B cell to a lymphoid organ,such as the tonsils or a lymph node, where there may be no antigen tosilence it. There, a robust immune/inflammatory response to thebacterial infection could activate this dangerous B cell and cause itto trigger an autoimmune disease.

"There have been reportslinking the onset of autoimmunity with a preceding bacterialinfection," said Stephen Gauld, Ph.D., lead author and post-doctoralfellow in Dr. Cambier's lab. "We are now conducting experiments todetermine the role of pro-inflammatory or bacterial products in theloss of B-cell anergy. We are also seeking to better understand theintracellular events that lead to anergy and its loss. Either of theselines of research could uncover potential targets for autoimmunetherapy."


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Materials provided by National Jewish Medical and Research Center. Note: Content may be edited for style and length.


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National Jewish Medical and Research Center. "Study Offers Clues To Origins Of Autoimmunity." ScienceDaily. ScienceDaily, 3 October 2005. <www.sciencedaily.com/releases/2005/10/051003082227.htm>.
National Jewish Medical and Research Center. (2005, October 3). Study Offers Clues To Origins Of Autoimmunity. ScienceDaily. Retrieved May 28, 2024 from www.sciencedaily.com/releases/2005/10/051003082227.htm
National Jewish Medical and Research Center. "Study Offers Clues To Origins Of Autoimmunity." ScienceDaily. www.sciencedaily.com/releases/2005/10/051003082227.htm (accessed May 28, 2024).

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