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Accelerating apoptosis, intracellular pathogens may use apoptotic neutrophils as a Trojan horse to infect other cells [ 24– 26].
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This highlights and confirms previous studies showing that in vivo generation of Tregs using apoptotic cell injection may be a useful tool to prevent and treat inflammatory autoimmune responses.
Although the notion that different T-cell subpopulations may preferentially use different pro- and anti-apoptotic pathways to regulate homeostasis has been previously proposed, no clear examples have been documented.
Furthermore, our data support the notion that a pharmaceutical drug-inhibiting Akt activity may not be sufficient to kill cancer cells on its own, but may be used to lower the apoptotic threshold and to resensitise chemoresistant tumours in combination treatment with defined chemotherapeutic drugs.
Currently, little is known about the pathophysiologic role of Pidd in clinical cancers, and whether Pidd expression may be used as a marker of apoptotic function that can guide cancer therapy.
If so, new experimental approaches, such as Bcl-2 homology domain 3 (BH3 -profiling, may BH3 -profilingover the anti-apoptotic barriers mayiating resistance.
These data suggest that such Bax inhibiting peptides from three mammalian species may be used to protect healthy cells from apoptotic injury under pathological conditions.
Alterations in cell membrane expression in apoptotic cells may be used to detect apoptosis in the laboratory.
In the future, ApoPep-1 conjugated with anti-apoptotic drugs may be used for targeted OA drug delivery.
Such cells are more likely to survive and may be cross-resistant to other drugs using the apoptotic pathway.
Beyond their use as vehicles to deliver resolving compounds (Metselaar et al, 2004), liposomes may also be used to mimic apoptotic cells to induce macrophage reprogramming.
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