Scientists at the Helmholtz Centre for Infection Research in Braunschweig, however, have studied on mice what happens when the normal interaction between these cells is disrupted: severe intestinal inflammation, whose symptoms closely resemble human autoimmune diseases, such as Morbus Crohn or Colitis ulcerosa.
"The intestinal surfaces form a border between the insides of the human body and the outside world, and they present our immune system with a monumental task," explains Dr. Astrid Westendorf, a researcher at the Helmholtz center. "Bacteria and other disease-causing pathogens that attempt to penetrate the body must be vehemently repelled at this point," she says. "On the other hand, nutrients, as well as the body's own cells and molecules, must not induce an immune reaction. Otherwise, a severe inflammation could result which might, in the long term, cause serious damage, and in some cases, even destroy the intestinal mucosa."
This is exactly what happens with so-called Villin HA-mice, which were studied by Westendorf and her colleagues. "These animals belong to a genetically altered strain that possess a molecule known as hemagglutinin, or HA, on the cells of their intestinal mucosa," she says. Westendorf injected these animals with immune cells from the blood of other mice strains that specifically produced immune cells targeting HA. The result: the immune cells attacked the intestinal surface and induced dramatic symptoms similar to those of patients with chronic intestinal inflammation.
A Surprising Tolerance
Westendorf. They keep the defense cells in check, most of which are the CD4+ or CD8+ type T cells, since these would otherwise attack the always present components of their own intestinal surface.
"The constant interaction between aggressive T cells and inhibiting TREG keeps the immunological balance of our intestinal mucosa intact," explains Prof. Dr. Jan Buer, work group leader at the Helmholtz Centre for Infection Research. "Many chronic, inflammatory intestinal ailments occur because this balance no longer functions," he says. Buer hopes that a better understanding of the processes involved could open up opportunities to selectively turn immune system responses up or down. "That," he says, "could lead to possible therapies for autoimmune diseases, like Morbus Crohn, but also tumors and infections in which the immune reaction needs to be selectively activated."
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