The figure shows the localization of IkBNS in the cell. IkBNS molecules (green) occur in dotted structures within the cell nucleus (blue). The function of these structures is, however, largely unknown.
HZI / Schmitz
A certain type of immune cell – the regulatory T cell, or Treg for short – is in charge of putting on the brakes on the immune response. In a way, this cell type might be considered the immune system’s traffic cop.Now, scientists at the Helmholtz Centre for Infection Research (HZI) have looked into the origin of Tregs and uncovered a central role played by the protein IκBNS. Armed with this knowledge, the researchers hope to manipulate Tregs in order to either inhibit or activate the immune system. Biochemist Prof. Ingo Schmitz and his team have now published their findings in the scientific journal Immunity.
Essentially, these are cells capable of constraining inflammation – even though IκBNS in no way influences the function of regulatory T cells," explains Dr. Marc Schuster, one of Schmitz' colleagues at HZI and the article’s first author. The researchers tested their hypothesis regarding IκBNS’ central role in Treg development in mice that are missing this factor. Since cells that lack IκBNS do not "become cops," the immune system's effector cells are undamped and could trigger chronic inflammation of the intestine.The results have confirmed that further research on IκBNS is of interest from a medical perspective as well. On the one hand, it allows predicting diseases: If IκBNS is fraught with errors, this could trigger autoimmune disorders. On the other hand, one potential therapeutic goal might be "to manipulate IκBNS in such a way that we can control the number of Tregs," explains Schmitz, who, in addition to his HZI research, also has a chair at the Otto von Guericke University Magdeburg. "IκBNS stabilization could benefit autoimmune disease therapy. As far as infections or tumors are concerned, we would need to inhibit IκBNS to decrease the number of regulatory T cells. Of course, all that is still in the very distant future." But because IκBNS also plays an important role in effector cell activation, an intervention might have unforeseen consequences. "This is a challenge you face with many different therapeutic targets," adds Schmitz.
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