Apoptosis

Apoptosis is a regulated form of cell death in which a cell dismantles itself and is usually cleared without provoking inflammation in surrounding tissue.

Caspase: A protease that cleaves specific proteins and helps execute programmed cell death. Executioner caspases dismantle cellular structures after apoptotic signaling activates them.
Death receptor: A cell-surface receptor that can initiate apoptosis after binding a death ligand. Death receptors provide the membrane entry point for the extrinsic pathway.
Necrosis: Cell death involving loss of membrane integrity and often inflammation in surrounding tissue. Unlike typical apoptosis, necrosis commonly releases cellular contents into tissue.
Embryonic development: The process by which an embryo forms and organizes its tissues and organs. Apoptosis removes selected cells to sculpt structures during development.
Efferocytosis: The recognition and engulfment of apoptotic cells by phagocytes or neighboring cells. Rapid efferocytosis prevents apoptotic cell remnants from becoming inflammatory debris.
Intrinsic apoptosis pathway: A cell-death signaling pathway initiated by internal stress and regulated by mitochondrial proteins. This pathway links DNA damage and other internal stresses to mitochondrial release of death factors.
Cytochrome c: A mitochondrial protein that transfers electrons in respiration and can activate apoptosome formation when released into the cytosol. Its release connects mitochondrial damage to caspase activation.
Necroptosis: A regulated form of lytic cell death that uses signaling proteins including RIPK3 and MLKL. It is regulated like apoptosis but ends with membrane rupture and inflammatory consequences.
Negative selection: The elimination of developing lymphocytes that strongly recognize self-antigens. Apoptosis removes many self-reactive immune cells during lymphocyte development.
Immune tolerance: The immune system's ability to avoid harmful responses against self and selected harmless targets. Clearance of apoptotic material can present self-antigens in a noninflammatory context.

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