In a new study, published in the Journal of Clinical Investigation Insights, August 3, 2017, the Crisa lab uncovered a novel function of a subset of macrophages, marked by the expression of the chemokine receptor CCR2, that foster pancreatic islet cell growth and maturation. The work, featured in the front page of the journal, demonstrates that loss of this myeloid cell population leads to a striking reduction in pancreatic β cell proliferation during the perinatal stage of islet expansion, and defective functional maturation that results in glucose intolerance. The investigators also demonstrate that populations of CCR2+ cells present in the adult bone marrow can rescue these defects. These findings harbor significant translational value for the design of cell-based therapies to promote pancreatic islet cell growth and regeneration in diabetes, and possibly in other degenerative diseases in which a defective tissue growth and regeneration may be rescued by this specialized type of macrophages.
Read the full article here: https://insight.jci.org/articles/view/93834
JCI Insight. 2017;2(15):e93834. https://doi.org/10.1172/jci.insight.93834.
We are grateful to Marshall Horwitz (University of Washington) and Bruce Torbett (The Scripps Research Institute) for their critical reading and insightful comments on this manuscript. This work was funded by a Life Sciences Discovery Fund program project grant to LC and VC, by a research fellowship from the Diabetes Research Connection to KM, in part by NIH grant R01 AI093808 to TMH, and through the NIH/National Cancer Institute Cancer Center Support Grant P30 CA008748 to Memorial Sloan Kettering Cancer Center. This work was partly funded by Medical University of South Carolina start-up funds to GH. The authors also acknowledge support from the Genomics Shared Resource, Hollings Cancer Center, Medical University of South Carolina. This shared resource is supported in part by the Hollings Cancer Center, Medical University of South Carolina Support Grant (P30 CA 138313).