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Live intracellular bacterial pathogens can transfer from infected cells to uninfected macrophages upon cell-to-cell contact.

Prion-like transfer of mutant huntingtin aggregates from presynaptic to postsynaptic neurons is enhanced by neuronal silencing and requires passage through the cytoplasm of Draper-expressing phagocytic glia in adult Drosophila brains.

Understanding communication mechanisms between unicellular parasites is crucial in the development of novel therapies, as they rely on diverse modes of communication (like extracellular vesicle release, cytoneme, and filopodia formation) to regulate their behavior and survival.

A lack of ADAM10-mediated shedding increases prion protein levels at the plasma membrane and promotes the generation of pathological prion proteins, which accelerates prion disease in mice.

A new type of mRNAs-loaded CD133⁺ vesicles, named intercellsome, mediate cell-cell communications to compensate intracellular proliferative signal deficit, representing a previously unrecognized mechanism of cell proliferation under stress.