@article{10.1172/jci.insight.93834, author = {Kristin Mussar AND Stephanie Pardike AND Tobias M. Hohl AND Gary Hardiman AND Vincenzo Cirulli AND Laura Crisa}, journal = {JCI Insight}, publisher = {The American Society for Clinical Investigation}, title = {A CCR2+ myeloid cell niche required for pancreatic β cell growth}, year = {2017}, month = {8}, volume = {2}, url = {https://insight.jci.org/articles/view/93834}, abstract = {Organ-specific patterns of myeloid cells may contribute tissue-specific growth and/or regenerative potentials. The perinatal stage of pancreas development marks a time characterized by maximal proliferation of pancreatic islets, ensuring the maintenance of glucose homeostasis throughout life. Ontogenically distinct CX3CR1+ and CCR2+ macrophage populations have been reported in the adult pancreas, but their functional contribution to islet cell growth at birth remains unknown. Here, we uncovered a temporally restricted requirement for CCR2+ myeloid cells in the perinatal proliferation of the endocrine pancreatic epithelium. CCR2+ macrophages are transiently enriched over CX3CR1+ subsets in the neonatal pancreas through both local expansion and recruitment of immature precursors. Using CCR2-specific depletion models, we show that loss of this myeloid population leads to a striking reduction in β cell proliferation, dysfunctional islet phenotypes, and glucose intolerance in newborns. Replenishment of pancreatic CCR2+ myeloid compartments by adoptive transfer rescues these defects. Gene profiling identifies pancreatic CCR2+ myeloid cells as a prominent source of IGF2, which contributes to IGF1R-mediated islet proliferation. These findings uncover proproliferative functions of CCR2+ myeloid subsets and identify myeloid-dependent regulation of IGF signaling as a local cue supporting pancreatic proliferation.}, number = {15}, doi = {10.1172/jci.insight.93834}, url = {https://doi.org/10.1172/jci.insight.93834}, }