In:
eLife, eLife Sciences Publications, Ltd, Vol. 3 ( 2014-12-29)
Kurzfassung:
The immune system protects the body from dangerous microbes and removes damaged cells. However, in some cases, the immune system can malfunction and attack healthy tissues, which can lead to type-1 diabetes, multiple sclerosis, and other autoimmune diseases. Many of the current treatments for these disorders suppress the immune system, which can make the individuals more susceptible to infections. It may be possible to treat autoimmune diseases using small pieces of protein—called peptides—that are based on proteins found on the cells that the immune system attacks by mistake. This strategy would target the specific immune cells that are malfunctioning, but allow the rest of the immune system to continue to work as normal. Peptide-based therapies for autoimmune diseases are currently being tested in clinical trials, and although the results look promising, it is not known precisely how they work. McPherson et al. used mice that develop a disease similar to multiple sclerosis because some of their immune cells, known as effector T cells, attack a protein found in the mouse brain called MBP. The mice were treated with a peptide based on part of MBP, which prevented them from developing the autoimmune disease. The success of the peptide therapy depended on the T cells producing large amounts of a protein called PD-1. This protein stops the T-cells from activating immune responses when they detect the MBP protein. The gene that makes PD-1 can have a methyl-tag—a chemical modification to DNA—which alters how much PD-1 is made in the T cells. When the gene has this methyl-tag, it can only be switched on for a short time to make a small amount of PD-1, which helps to control the immune responses activated by the T cell. However, when the methyl-tag was removed as a result of the peptide therapy the gene could be switched on for much longer, so that much more PD-1 was produced. This work helps us to understand how peptide therapy works and should improve the chances of using this therapy to successfully treat patients with autoimmune diseases.
Materialart:
Online-Ressource
ISSN:
2050-084X
DOI:
10.7554/eLife.03416.001
DOI:
10.7554/eLife.03416.002
DOI:
10.7554/eLife.03416.003
DOI:
10.7554/eLife.03416.004
DOI:
10.7554/eLife.03416.005
DOI:
10.7554/eLife.03416.006
DOI:
10.7554/eLife.03416.007
DOI:
10.7554/eLife.03416.008
DOI:
10.7554/eLife.03416.009
DOI:
10.7554/eLife.03416.010
DOI:
10.7554/eLife.03416.011
DOI:
10.7554/eLife.03416.012
DOI:
10.7554/eLife.03416.013
DOI:
10.7554/eLife.03416.014
DOI:
10.7554/eLife.03416.015
DOI:
10.7554/eLife.03416.016
DOI:
10.7554/eLife.03416.017
DOI:
10.7554/eLife.03416.018
DOI:
10.7554/eLife.03416.019
DOI:
10.7554/eLife.03416.020
DOI:
10.7554/eLife.03416.021
DOI:
10.7554/eLife.03416.022
DOI:
10.7554/eLife.03416.023
DOI:
10.7554/eLife.03416.024
Sprache:
Englisch
Verlag:
eLife Sciences Publications, Ltd
Publikationsdatum:
2014
ZDB Id:
2687154-3
