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Review
. 1998 Jan;72(1):1-9.
doi: 10.1128/JVI.72.1.1-9.1998.

The relative role of lymphocyte granule exocytosis versus death receptor-mediated cytotoxicity in viral pathophysiology

M J Smyth  1 , J A Trapani
Affiliations
Review

The relative role of lymphocyte granule exocytosis versus death receptor-mediated cytotoxicity in viral pathophysiology

M J Smyth et al. J Virol. 1998 Jan.
No abstract available

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Figures

FIG. 1
FIG. 1
Viral inhibition of endogenous and CL-induced apoptotic pathways. Viruses can subvert the intrinsic apoptotic pathway by interfering with virtually every aspect of the cascade so far defined. Many viral strategies involve protease inhibitors (CrmA, p35, IAP, etc.) that can block a spectrum of cysteine protease caspases or inhibit signal transduction through Fas, FADD, or FLICE. Viral Bc1-2-like molecules (v-bc1-2) can also block activation of the caspase cascade by interfering with normal Bc1-2-like molecules that control apoptosis at the outer mitochondrial membrane. In addition, viruses evade immune detection by a variety of means, including inhibiting the loading of viral peptides onto MHC by TAP transporters, inducing degradation of MHC (by stealth proteins), or producing their own decoy MHC (HLA) molecules that bind NK cell inhibitory receptors and inhibit NK cytotoxicity. As yet, a specific viral inhibitor of perforin has not been described. Viral inhibitors can, in principle, block all Fas-mediated apoptotic events; however, CL do trigger target cell death through putative cytoplasmic and/or cell membrane granzyme substrates that do not depend on caspase activation. Abbreviations: er, endoplasmic reticulum; GrB, granzyme B; HLA, human leukocyte antigen.
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References

    1. Ahn K, Gruhler A, Galocha B, Jones T R, Wiertz E J, Ploegh H L, Peterson P A, Yang Y, Fruh K. The ER-luminal domain of the HCMV glycoprotein US6 inhibits peptide translocation by TAP. Immunity. 1997;6:613–621. - PubMed
    1. Ando K, Hiroishi K, Kaneko T, Moriyama T, Muto Y, Kayagaki N, Yagita H, Okumura K, Imawari M. Perforin, Fas/Fas ligand, and TNF-α pathways as specific and bystander killing mechanisms of hepatitis C virus-specific human CTL. J Immunol. 1997;158:5283–5291. - PubMed
    1. Anel A, Buferne M, Boyer C, Schmitt-Verhulst A-M, Golstein P. T cell receptor-induced Fas ligand expression in cytotoxic T lymphocyte clones is blocked by protein tyrosine kinase inhibitors and cyclosporin A. Eur J Immunol. 1994;24:2469–2476. - PubMed
    1. Arase H, Arase N, Saito T. Fas-mediated cytotoxicity by freshly isolated natural killer cells. J Exp Med. 1995;181:1235–1238. - PMC - PubMed
    1. Ashwell J D, Klausner R D. Genetic and mutational analysis of the T cell antigen receptor. Annu Rev Immunol. 1990;8:139–167. - PubMed

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