Joseph A. Trapani

Cytotoxic cell granule-mediated apoptosis: perforin delivers granzyme B-serglycin complexes into target cells without plasma membrane pore formation.

Functional role of phosphatidylinositol 3-kinase in direct tumor lysis by human natural killer cells.

Suppression of lymphoma and epithelial malignancies effected by interferon gamma.

Tumor-mediated apoptosis of cancer-specific T lymphocytes--reversing the "kiss of death"?

Functional significance of the perforin/granzyme cell death pathway.

Single-chain antigen recognition receptors that costimulate potent rejection of established experimental tumors.

Rejection of syngeneic colon carcinoma by CTLs expressing single-chain antibody receptors codelivering CD28 costimulation.

A clathrin/dynamin- and mannose-6-phosphate receptor-independent pathway for granzyme B-induced cell death.

Expression of IFI 16 in epithelial cells and lymphoid tissues.

Caspase activation by granzyme B is indirect, and caspase autoprocessing requires the release of proapoptotic mitochondrial factors.

Purification of natural killer cell cytotoxic granules for assaying target cell apoptosis.

Cutting edge: granzymes A and B are not essential for perforin-mediated tumor rejection.

Novel mechanisms of apoptosis induced by histone deacetylase inhibitors.

Granzyme B: pro-apoptotic, antiviral and antitumor functions.

hScrib is a functional homologue of the Drosophila tumour suppressor Scribble.

Granzyme B encoded by the commonly occurring human RAH allele retains pro-apoptotic activity.

Granzyme M mediates a novel form of perforin-dependent cell death.

A functional role for CD28 costimulation in tumor recognition by single-chain receptor-modified T cells.

Discordant regulation of granzyme H and granzyme B expression in human lymphocytes.

Assaying cytochrome C translocation during apoptosis.

Cytotoxic activity of the lymphocyte toxin granzyme B.

Gene-engineered T cells as a superior adjuvant therapy for metastatic cancer.

Cytotoxic lymphocytes; instigators of dramatic target cell death.

The functional basis for hemophagocytic lymphohistiocytosis in a patient with co-inherited missense mutations in the perforin (PFN1) gene.

A central role for Bid in granzyme B-induced apoptosis.

Calcium-dependent plasma membrane binding and cell lysis by perforin are mediated through its C2 domain: A critical role for aspartate residues 429, 435, 483, and 485 but not 491.

Biochemical and growth regulatory activities of the HIN-200 family member and putative tumor suppressor protein, AIM2.

A functional analysis of the putative polymorphisms A91V and N252S and 22 missense perforin mutations associated with familial hemophagocytic lymphohistiocytosis.

Interaction of the nuclear localizing cytolytic granule serine protease granzyme B with importin alpha or beta: modulation by the serpin inhibitor PI-9.

Extracellular matrix remodeling by human granzyme B via cleavage of vitronectin, fibronectin, and laminin.

Adoptive transfer of gene-engineered CD4+ helper T cells induces potent primary and secondary tumor rejection.

Cationic sites on granzyme B contribute to cytotoxicity by promoting its uptake into target cells.

The dual adverse effects of TGF-beta secretion on tumor progression.

Adoptive transfer of T cells modified with a humanized chimeric receptor gene inhibits growth of Lewis-Y-expressing tumors in mice.

Report on apoptosis and immunity, 31 May-3 June 2005, Palm Cove, Queensland, Australia.

Addressing the mysteries of perforin function.

Role of Bid-induced mitochondrial outer membrane permeabilization in granzyme B-induced apoptosis.

A critical role for granzyme B, in addition to perforin and TNFalpha, in alloreactive CTL-induced mouse pancreatic beta cell death.

Perforin and Fas induced by IFNgamma and TNFalpha mediate beta cell death by OT-I CTL.

Cytotoxic T lymphocyte-induced killing in the absence of granzymes A and B is unique and distinct from both apoptosis and perforin-dependent lysis.

Granzyme B-mediated death of pancreatic beta-cells requires the proapoptotic BH3-only molecule bid.

Cytotoxic T lymphocytes from cathepsin B-deficient mice survive normally in vitro and in vivo after encountering and killing target cells.

Cytotoxic T-cells from T-cell receptor transgenic NOD8.3 mice destroy beta-cells via the perforin and Fas pathways.

A novel c-Jun-dependent signal transduction pathway necessary for the transcriptional activation of interferon gamma response genes.

The major human and mouse granzymes are structurally and functionally divergent.

Ligation of the cell surface receptor, CD46, alters T cell polarity and response to antigen presentation.

Perforin-mediated target-cell death and immune homeostasis.

Residual active granzyme B in cathepsin C-null lymphocytes is sufficient for perforin-dependent target cell apoptosis.

Apoptosis induced by the lymphocyte effector molecule perforin.

The complex issue of regulating perforin expression.

Perforin activity and immune homeostasis: the common A91V polymorphism in perforin results in both presynaptic and postsynaptic defects in function.

The granzyme B gene is highly polymorphic in wild mice but essentially invariant in common inbred laboratory strains.

Infective, neoplastic, and homeostatic sequelae of the loss of perforin function in humans.

A common fold mediates vertebrate defense and bacterial attack.

H is for helper: granzyme H helps granzyme B kill adenovirus-infected cells.

Cloning and characterisation of Ifi206: a new murine HIN-200 family member.

Sustained antigen-specific antitumor recall response mediated by gene-modified CD4+ T helper-1 and CD8+ T cells.

Measuring cell death mediated by cytotoxic lymphocytes or their granule effector molecules.

The role of p202 in regulating hematopoietic cell proliferation and differentiation.

The MACPF/CDC family of pore-forming toxins.

Granzyme K expressing cytotoxic T lymphocytes protects against influenza virus in granzyme AB-/- mice.

A renaissance in understanding the multiple and diverse functions of granzymes?

Dihydrofuro[3,4-c]pyridinones as inhibitors of the cytolytic effects of the pore-forming glycoprotein perforin.

Perforin-mediated suppression of B-cell lymphoma.

The Lewis-Y carbohydrate antigen is expressed by many human tumors and can serve as a target for genetically redirected T cells despite the presence of soluble antigen in serum.

The molecular basis for perforin oligomerization and transmembrane pore assembly.

Temperature sensitivity of human perforin mutants unmasks subtotal loss of cytotoxicity, delayed FHL, and a predisposition to cancer.

Cutting edge: rapid and efficient in vivo cytotoxicity by cytotoxic T cells is independent of granzymes A and B.

Proteolytic activation of the cytotoxic phenotype during human NK cell development.

The battlefield of perforin/granzyme cell death pathways.

Endolysosomal proteases and their inhibitors in immunity.

Incentives: encouraging adventurous ideas.

Cathepsin H is an additional convertase of pro-granzyme B.

Functional crosstalk between type I and II interferon through the regulated expression of STAT1.

Human and mouse perforin are processed in part through cleavage by the lysosomal cysteine proteinase cathepsin L.

Perforin: structure, function, and role in human immunopathology.

Functional dissection of the granzyme family: cell death and inflammation.

A role for granzyme M in TLR4-driven inflammation and endotoxicosis.

Proteases in lymphocyte killer function: redundancy, polymorphism and questions remaining.

Cathepsin C limits acute viral infection independently of NK cell and CD8+ T-cell cytolytic function.

The immunostimulatory effect of lenalidomide on NK-cell function is profoundly inhibited by concurrent dexamethasone therapy.

The structural basis for membrane binding and pore formation by lymphocyte perforin.

Tumor ablation by gene-modified T cells in the absence of autoimmunity.

Homeostatic defects in interleukin 18-deficient mice contribute to protection against the lethal effects of endotoxin.

Protection from endogenous perforin: glycans and the C terminus regulate exocytic trafficking in cytotoxic lymphocytes.

Inhibition of the cellular function of perforin by 1-amino-2,4-dicyanopyrido[1,2-a]benzimidazoles.

A critical role for granzymes in antigen cross-presentation through regulating phagocytosis of killed tumor cells.

Fatal immune dysregulation due to a gain of glycosylation mutation in lymphocyte perforin.

Inhibition of the pore-forming protein perforin by a series of aryl-substituted isobenzofuran-1(3H)-ones.

Activated mouse B cells lack expression of granzyme B.

Perforin evolved from a gene duplication of MPEG1, followed by a complex pattern of gene gain and loss within Euteleostomi.

Protecting a serial killer: pathways for perforin trafficking and self-defence ensure sequential target cell death.

A novel role for granzymes in anti-tumor immunity.

Granzyme B is dispensable in the development of diabetes in non-obese diabetic mice.

Surprisingly variable "dangers, toils, and snares" faced by humans and mice.

Perforin forms transient pores on the target cell plasma membrane to facilitate rapid access of granzymes during killer cell attack.

Cloning and characterising an unusual perforin from chicken (Gallus gallus).

Human perforin mutations and susceptibility to multiple primary cancers.

Persistence and efficacy of second generation CAR T cell against the LeY antigen in acute myeloid leukemia.

Rapid and unidirectional perforin pore delivery at the cytotoxic immune synapse.

Defining the interaction of perforin with calcium and the phospholipid membrane.

Exploration of a series of 5-arylidene-2-thioxoimidazolidin-4-ones as inhibitors of the cytolytic protein perforin.

Perforinopathy: a spectrum of human immune disease caused by defective perforin delivery or function.

B-CLL cells acquire APC- and CTL-like phenotypic characteristics after stimulation with CpG ODN and IL-21.

The perforin pore facilitates the delivery of cationic cargos.

Granzyme h is a novel protease expressed by human mast cells.

A Method for Detecting Intracellular Perforin in Mouse Lymphocytes.

TRAIL(+) NK Cells Control CD4(+) T Cell Responses during Chronic Viral Infection to Limit Autoimmunity.