Published in:
01-01-2018 | Commentary
When beta cells talk back
Published in: Diabetologia | Issue 1/2018
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Islet macrophages reside in the perivascular space next to islet blood vessels. They are long-lived and self-renewing, maintaining about two to ten macrophages per islet [1]. However, more than three decades after the first description of islet macrophages [2], our knowledge regarding the biological role of these cells is limited (reviewed in [3]). Emerging evidence indicates that islet macrophages are important for islet homeostasis and secrete numerous factors that modulate beta cell activity. Reciprocally, in this issue of Diabetologia, Weitz et al demonstrate that a factor secreted by beta cells is sensed by islet macrophages [4], revealing the possibility of a physiological, two-way dialogue between islet macrophages and pancreatic beta cells (Fig. 1).
Fig. 1
Crosstalk between beta cells and islet macrophages. In response to various stimuli originating within and outside of the islet, macrophages release signals that influence beta cell function. IL-1β and TNF-α are released by macrophages under inflammatory and postprandial conditions; these act on the beta cell to alter insulin production and secretion and, with chronic exposure, can lead to beta cell dysfunction. Several regenerative factors, which promote beta cell proliferation, including EGF and TGF-β1, are released by islet macrophages in response to beta cell loss. Likewise, beta cells release signals that act on islet macrophages. In diabetes IAPP aggregates originating from beta cells activate inflammatory responses in macrophages. In this issue, Weitz et al [4] demonstrate that ATP, co-released from beta cells during insulin secretion, is sensed by macrophages. The outcome of this signal on macrophage function is unknown. Additional signals may exist between islet macrophages and beta cells that have not yet been identified
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