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The molecular mechanisms underlying inflammatory bowel diseases remain currently not completely understood, and therapeutic options are scarce.
Herein, we have identified that a normally endoplasmic reticulum resident protein, AGR2, exhibits tightly regulated secretion mechanisms that are perturbed in Crohn’s disease. We demonstrate that the extracellular release of AGR2 leads to the chemoattraction of monocytes, thereby suggesting extracellular AGR2’s pro‐inflammatory functions, that can be blocked using specific antibodies.
As a consequence, this discovery could represent an appealing therapeutic approach to attenuate the inflammatory burden in Crohn’s disease.