Amanda J. Lanser

TL;DR: It is found that TGF-β was required for the in vitro development of microglia that express the microglial molecular signature characteristic of adultmicroglia and that microglian were absent in the CNS of TGF -β1–deficient mice.

TL;DR: The results suggest that recruitment of inflammatory monocytes plays an important role in disease progression and that modulation of these cells is a potential therapeutic approach.

TL;DR: Corrigendum: Identification of a unique TGF-β–dependent molecular and functional signature in microglia and its role in cell reprograming is identified.

TL;DR: It is found that anti-LAP antibody, which targets the latency-associated peptide (LAP)/transforming growth factor–β (TGF-β) complex on Tregs and other cells, enhances antitumor immune responses and reduces tumor growth in models of melanoma, colorectal carcinoma, and glioblastoma.

TL;DR: It is reported that acute and synchronous microglia depletion and subsequent repopulation induces gray matter microgliosis, neuronal death in the somatosensory cortex and ataxia-like behavior.