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Review
. 2004 Jun;16(3):271-6.
doi: 10.1016/j.coi.2004.03.020.

Apoptosis and loss of virus-specific CD8+ T-cell memory

Raymond M Welsh  1 , Kapil Bahl, Xiaoting Z Wang
Affiliations
Review

Apoptosis and loss of virus-specific CD8+ T-cell memory

Raymond M Welsh et al. Curr Opin Immunol. 2004 Jun.

Abstract

CD8(+) T-cell memory to viruses is stable in the absence but volatile in the presence of other infections. Apoptotic events that occur early in acute infections delete pre-existing memory T cells, leaving the host with reduced memory (except for cross-reactive responses) to previously encountered viruses. Apoptotic events also silence the acute immune response, leaving the host with a residual population of memory T cells. Persistent infections can induce apoptotic deletions of memory T cells that are specific to the persisting virus and to previously encountered pathogens.

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Figures

Figure 1
Figure 1
CD8+ T-cell proliferation and apoptosis during acute viral infection. This graft reflects data generated in the LCMV system, showing the magnitude of type 1 IFN, virus load, and frequencies of cross-reactive and non-cross-reactive memory T cells as a new T-cell response is generated. Pre-existing memory cells are driven into apoptosis, but cross-reactive cells ultimately expand and are preserved or increased in memory. Virus-specific T cells undergo apoptosis during the silencing phase, but those expressing IL-7Rα and not reacting with Annexin V survive this process and enter the long-term memory pool.
Figure 2
Figure 2
Progression of clonal exhaustion during persistent infection. This figure, based on persistent LCMV infections, induced by infecting adult mice with high doses of widely disseminating virus, depicts an epitope-specificity-based functional exhaustion or complete deletion of T cells. Prior to deletion, T cells lose functions in a prescribed order, as depicted for GP33-specific T cells. NP396-specific T cells will also lose function, but depicted here is their propensity to be completely eliminated, presumably by apoptotic mechanisms, which are, in part, controlled by Fas/FasL and TNFα.
See this image and copyright information in PMC

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References

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