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Fig. 1 | European Journal of Medical Research

Fig. 1

From: Both extracellular vesicles from helicobacter pylori-infected cells and helicobacter pylori outer membrane vesicles are involved in gastric/extragastric diseases

Fig. 1

The biogenesis of EVs. The cytoplasmic membrane first invaginates exosomes to form early endo nucleosomes, which further develop into late endo nucleosomes, and then the endo nucleosome membrane invaginates to form multivesicular bodies (MVBs). MVB are produced in two ways. On one hand, they can fuse with lysosomes and be degraded. On the other hand, MVBs fuse with the cell membrane and release their encapsulated luminal vesicles into the extracellular space, thus forming exosomes. The exosomes are released and can interact with the recipient cell via cell signaling molecules on their surface. Exosomes can also act by different mechanisms such as endocytosis, phagocytosis or direct fusion with the cell membrane into the recipient cell. Microvesicles are formed through direct outward budding and shedding from the plasma membrane. Apoptotic bodies(ABs) are small membranous particles released during programmed cell death

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