In:
eLife, eLife Sciences Publications, Ltd, Vol. 2 ( 2013-05-14)
Abstract:
One of the main roles of the spleen is to make the antibodies that protect the body against viruses, bacteria and other microorganisms. Antibodies are made by B cells, which are a type of white blood cell, after they have been exposed to antigens. For most antibody responses, it is also necessary for the B cells to get help from other white blood cells called T cells that have been exposed to antigens. Specialized cells called dendritic cells have a central role in bringing the antigens—which are usually fragments of the infectious agents that have invaded the body—to the T cells. One subset of dendritic cells, called CD4+ dendritic cells, are found in large numbers in a part of the spleen called the bridging channel, but the process by which these cells become localized in this channel has not been fully understood. Now, Yi and Cyster show that a receptor called EBI2, which is found on the surface of CD4+ dendritic cells, binds to a type of organic molecule called an oxysterol that is produced in the bridging channel. In mice that had been genetically engineered to lack EBI2 or the enzymes needed to make this particular oxysterol—which is known as 7α,25-dihydroxycholesterol, or 7α,25-OHC for short—the CD4+ dendritic cells were no longer clustered in the bridging channel and their number was markedly decreased. This showed that the interaction between EBI2 and the oxysterol was essential for ensuring that the CD4+ dendritic cells were in the right place. The correct positioning of the CD4+ dendritic cells was, in turn, necessary for maintaining cell numbers. Moreover, these mice had a weakened immune response because of the very low number of antigens that were being presented to the T cells. A number of autoimmune diseases, such as lupus, are caused by the body developing an immune response to its own cells and tissues. One implication of the work of Yi and Cyster is that if small molecule inhibitors of EBI2 could be designed, they might be able to suppress the onset of such autoimmune responses.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.00757.001
DOI:
10.7554/eLife.00757.002
DOI:
10.7554/eLife.00757.003
DOI:
10.7554/eLife.00757.004
DOI:
10.7554/eLife.00757.005
DOI:
10.7554/eLife.00757.006
DOI:
10.7554/eLife.00757.007
DOI:
10.7554/eLife.00757.008
DOI:
10.7554/eLife.00757.009
DOI:
10.7554/eLife.00757.010
DOI:
10.7554/eLife.00757.011
DOI:
10.7554/eLife.00757.012
DOI:
10.7554/eLife.00757.013
DOI:
10.7554/eLife.00757.014
DOI:
10.7554/eLife.00757.015
DOI:
10.7554/eLife.00757.016
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2013
detail.hit.zdb_id:
2687154-3
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