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With a lack of mitochondria, can red blood cells perform intrinsic apoptosis and do they have another way of generating cytochrome c to attach to a CARD domain and assemble the apoptosome?

Or are they dependent on killer lymphocytes to bind via the fas ligand and activate procaspase 8 or 10 in extrinsic apoptosis? Do red blood cells even have fas ligand receptors for this process?

Or is there an entirely different method for red blood cells?

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No expert, but I thought that red blood cells were relatively inert, and were essentially killed/recycled by the immune system after their useful lifespan. How this is determined I don't know, but I am interested to hear the answer to this question. –  Luke Jul 16 '12 at 13:11
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Red blood cells (RBCs) don't have nuclei in mammals, so they are usually considered to be pretty inert compared to other cells.

They do have some biochemical activity, and evidently there is some mechanism for cell death in RBCs when they are induced to degrade or infected by pathogens. I found this reference that shows caspases -8 and -3 are evident in mature RBCs. Several other components of the cell death pathway are not evident.

At this time the authors speculate that they don't activate to induce cell death.

It seems that over the broad field of disease research 'apoptosis' and 'cell death' are used equivalently even when the well known apoptosis pathway is not involved.

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Senescent red blood cells are cleared by macrophages in a process called eryptosis or is better known as erythrocyte programmed cell death or apoptosis. The mechanism is excellently reviewed here. In summary it is mediated by caspases, phospholipase A and prostaglandin E.

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