Considering Fas ligand as a target for therapy

Bibliography

• SUDA T, TAKAHASHI T, GOLSTEIN P, NAGATA S: Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family. CO (1993) 75:1169–1178.
   Google Scholar
• •Key reference on cloning and expression of FasL.
   Google Scholar
• JANSSEN O, SANZENBACHER R, KABELITZ D: Regulation of activation-induced cell death of mature T-lymphocyte populations. Cell Tissue Res. (2000) 301:85–99.
   PubMed Web of Science ®Google Scholar
• KRAMMER PH: CD95(AP0-1/Fas)-mediated apoptosis: live and let die. Adv. Immunol. (1999) 71:163–210.
   PubMedGoogle Scholar
• ••Comprehensive review on Fas-mediatedapoptosis.
   Google Scholar
• NAGATA S: Fas ligand-induced apoptosis. Ann. Rev. Genet. (1999) 33:29–55.
   PubMed Web of Science ®Google Scholar
• ••Comprehensive review on FasL-inducedapoptosis.
   Google Scholar
• PETER ME, KRAMMER PH: The CD95(AP0-1/Fas) DISC and beyond. Cell Death Differ. (2003) 10:26–35.
   PubMed Web of Science ®Google Scholar
• ••Comprehensive review on signaltransduction during Fas-mediated apoptosis.
   Google Scholar
• PITTI RM, MARSTERS SA, LAWRENCE D A et al.: Genomic amplification of a decoy receptor for Fas ligand in lung and colon cancer. Nature (1998) 396:699–703.
   Google Scholar
• ROTH W, ISENMANN S, NAKAMURA M et al: Soluble decoy receptor 3 is expressed by malignant gliomas and suppresses CD95 ligand-induced apoptosis and chemotaxis. Cancer Res. (2001) 61:2759–2765.
   PubMed Web of Science ®Google Scholar
• ROUVIER E, LUCIANI ME GOLSTEIN P: Fas involvement in Ca(2-0-independent T cell-mediated cytotoxicity. J. Exp. Med. (1993) 177:195–200.
   PubMed Web of Science ®Google Scholar
• GRIFFITH T S, BRUNNER T, FLETCHER SM, GREEN DR, FERGUSON TA: Fas ligand-induced apoptosis as a mechanism of immune privilege. Science (1995) 270:1189–1192.
   PubMed Web of Science ®Google Scholar
• O'CONNELL J, HOUSTON A, BENNETT MW, O'SULLIVAN GC, SHANAHAN F: Immune privilege or inflammation? Insights into the Fas ligand enigma. Nat. Med. (2001) 7:271–274.
   PubMed Web of Science ®Google Scholar
• •Critical discussion on the role of FasL in the establishment of immune privilege.
   Google Scholar
• GREEN DR, FERGUSON TA: The role of Fas ligand in immune privilege. Nat. Rev. Mol. Cell Biol. (2001) 2:917–924.
   PubMed Web of Science ®Google Scholar
• FERGUSON TA, GREEN DR, GRIFFITH TS: Cell death and immune privilege. Int. Rev Immune] (2002) 21:153–172.
   PubMedGoogle Scholar
• •Critical discussion on the role of FasL In immune privilege.
   Google Scholar
• RESTIFO NP: Not so Fas: re-evaluating the mechanisms of immune privilege and tumor escape. Nat. Med. (2000) 6:493–495.
   PubMed Web of Science ®Google Scholar
• BELLGRAU D, GOLD D, SELAWRY H et al: A role for CD95 ligand in preventing graft rejection. Nature (1995) 377:630–632.
   PubMed Web of Science ®Google Scholar
• GIORDANO C, STASSI G, DE MARIA R et al.: Potential involvement of Fas and its ligand in the pathogenesis of Hashimoto's thyroiditis. Science (1997) 275:960–963.
   Google Scholar
• GOCHUICO BR, MIRANDA KM, HESSEL EM et al: Airway epithelial Fas ligand expression: potential role in modulating bronchial inflammation. Am. J. Physic] (1998) 274:L444–L449.
   Google Scholar
• HUNT JS, VASSMER D, FERGUSON TA, MILLER L: Fas ligand is positioned in mouse uterus and placenta to prevent trafficking of activated leukocytes between the mother and the conceptus. Immunol (1997) 158:4122–4128.
   Web of Science ®Google Scholar
• NAKAJIMA M, NAKAJIMA A, KAYAGAKI N et al.: Expression of Fas ligand and its receptor in cutaneous lupus: implication in tissue injury. Clin. Immunol Immunopathol (1997) 83:223–229.
   PubMedGoogle Scholar
• TAKADA T, NISHIDA K, DOITA M, KUROSAKA M: Fas ligand exists on intervertebral disc cells: a potential molecular mechanism for immune privilege of the disc. Spine (2002) 27:1526–1530.
   PubMed Web of Science ®Google Scholar
• SONG J, SAFI E, BROWN W et al: Roles of Fas and Fas ligand during mammary gland remodeling. Clin. Invest. (2000) 106:1209–1220.
   Google Scholar
• KOKKONEN TS, AUGUSTIN MT, MAKINEN JM, KOKKONEN J, KARTTUNEN TJ: High endothelial venules of the lymph nodes express Fas ligand. Histochem. Cytochem. (2004) 52:693–699.
   PubMed Web of Science ®Google Scholar
• DE MARIA R, ZEUNER A, ERAMO A et al.: Negative regulation of erythropoiesis by caspase-mediated cleavage of GATA- I. Nature (1999) 401:489–493.
   PubMed Web of Science ®Google Scholar
• KAPLAN HJ, LEIBOLE MA, TEZEL T, FERGUSON TA: Fas ligand (CD95 ligand) controls angiogenesis beneath the retina. Nat. Med. (1999) 5:292–297.
   PubMed Web of Science ®Google Scholar
• HILL LL, OUHTIT A, LOUGHLIN SM et al.: Fas ligand: a sensor for DNA damage
   Google Scholar
• •• critical in skin cancer etiology. Science (1999) 285:898–900.
   Google Scholar
• O'CONNELL J, BENNETT MW, O'SULLIVAN GC, COLLINS JK, SHANAHAN F: The Fas counterattack: cancer as a site of immune privilege. Immunol Today (1999) 20:46–52.
   PubMedGoogle Scholar
• VON BERNSTORFF W, SPANJAARD RA, CHAN AK et al.: Pancreatic cancer cells can evade immune surveillance via nonfunctional Fas (APO-1/CD95) receptors and aberrant expression of functional Fas ligand. Surgery (1999) 125:73–84.
   PubMed Web of Science ®Google Scholar
• RESTIFO NP: Countering the 'counterattack' hypothesis. Nat. Med. (2001) 7:259–274
   PubMed Web of Science ®Google Scholar
• •Critical discussion of the tumour counterattack hypothesis.
   Google Scholar
• IGNEY FH, KRAMMER PH: Immune escape of tumors: apoptosis resistance and tumor counterattack. Leukoc. Biol. (2002) 71:907–920.
   PubMed Web of Science ®Google Scholar
• •Critical discussion of the tomour counterattack hypothesis and other tumour escape mechanisms.
   Google Scholar
• RIVOLTINI L, CARRABBA M, HUBER V et al: Immunity to cancer: attack and escape in T lymphocyte-tumor cell interaction. Immunol. Rev. (2002) 188:97–113.
   PubMed Web of Science ®Google Scholar
• HOUSTON A, O'CONNELL J: The Fas signalling pathway and its role in the pathogenesis of cancer. Curr. Opin. Pharmacol. (2004) 4:321–326.
   PubMed Web of Science ®Google Scholar
• HALLERMALM K, DE GEER A, KIESSLING R, LEVITSKY V, LEVITSKAYA J: Autocrine secretion of Fas ligand shields tumor cells from Fas-mediated killing by cytotoxic lymphocytes. Cancer Res. (2004) 64:6775–6782.
   PubMed Web of Science ®Google Scholar
• WATANABE-FUKUNAGA R, BRANNAN CI, COPELAND NG, JENKINS NA, NAGATA S: Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis. Nature (1992) 356:314–317.
   PubMed Web of Science ®Google Scholar
• •First link of the 'lymphoproliferation (Ipi) phenotype' in mice to a mutation in the Fas receptor.
   Google Scholar
• ADACHI M, SUEMATSU S, SUDA T et al.: Enhanced and accelerated lymphoproliferation in Fas-null mice. Proc. Natl. Acad. Sci. USA (1996) 93:2131–2136.
   PubMed Web of Science ®Google Scholar
• RAMSDELL F, SEAMAN MS, MILLER RE et al.: glcligld mice are unable to express a functional ligand for Fas. Eur. Immunol (1994) 24:928–933.
   PubMed Web of Science ®Google Scholar
• •First demonstration that mice suffering from a generalised lymphoproliferative syndrome (Ipr) do not express a functional FasL.
   Google Scholar
• TAKAHASHI T, TANAKA M, BRANNAN CI et al: Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. Cell (1994) 76:969–976.
   PubMed Web of Science ®Google Scholar
• •Defines the FasL mutation that causes the generalised lymphoproliferative syndrome (Ipr) phenotype in mice.
   Google Scholar
• KARRAY S, KRESS C, CUVELLIER S et al.: Complete loss of Fas ligand gene causes massive lymphoproliferation and early death, indicating a residual activity of gld allele. J. Immunol (2004) 172:2118–2125.
   PubMed Web of Science ®Google Scholar
• •The more severe phenotype of FasL deficient, as compared to gld mice suggests additional relevant functions of FasL.
   Google Scholar
• CANALE VC, SMITH CH: Chronic lymphadenopathy simulating malignant lymphoma. J. Pediatr. (1967) 70:891–899.
   PubMed Web of Science ®Google Scholar
• FISHER GH, ROSENBERG FJ, STRAUS SE et al: Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome. Cell (1995) 81:935–946.
   PubMed Web of Science ®Google Scholar
• DRAPPA J, VAISHNAW AK, SULLIVAN KE, CHU J L, ELKON KB: Fas gene mutations in the Canale-Smith syndrome, an inherited lymphoproliferative disorder associated with autoimmunity. N Engl. J. Med. (1996) 335:1643–1649.
   PubMed Web of Science ®Google Scholar
• RIEUX-LAUCAT F, LE DEIST F, FISCHER A: Autoimmune lymphoproliferative syndromes: genetic defects of apoptosis pathways. Cell Death. Differ. (2003) 10:124–133.
   PubMed Web of Science ®Google Scholar
• RIEUX-LAUCAT F, FISCHER A, DEIST FL: Cell-death signaling and human disease. Curr. Opin. Immunol. (2003) 15:325–331.
   PubMed Web of Science ®Google Scholar
• WU J, WILSON J, HE J et al.: Fas ligand mutation in a patient with systemic lupus erythematosus and lymphoproliferative disease. J. Clin. Invest. (1996) 98:1107–1113.
   PubMed Web of Science ®Google Scholar
• •FasL mutations can be associated with SLE and lymphoproliferation in patients.
   Google Scholar
• LI-WEBER M, KRAMMER PH: Function and regulation of the CD95 (AP0-1/Fas) ligand in the immune system. Semiri. Immunol (2003) 15:145–157.
   PubMed Web of Science ®Google Scholar
• ••Comprehensive review on the functionand transcriptional regulation of FasL.
   Google Scholar
• GRONBAEK K, STRATEN PT, RALFKIAER E et al.: Somatic Fas mutations in non-Hodgkin's lymphoma: association with extranodal disease and autoimmunity. Blood (1998) 92:3018–3024.
   PubMed Web of Science ®Google Scholar
• KIM HS, LEE SH, LEE JW et al.: Mutational analysis of Fas ligand gene in human non-Hodgkin lymphoma. APMIS (2003) 111:490–496.
   PubMed Web of Science ®Google Scholar
• OBERG HH, LENGL-JANSSEN B, ROBERTSON MJ, KABELITZ D, JANSSEN O: Differential role of tyrosine phosphorylation in the induction of apoptosis in T cells via CD95 or the TCR/CD3-complex. Cell Death. Differ. (1997) 4:403–412.
   PubMed Web of Science ®Google Scholar
• OBERG HH, SANZENBACHER R, LENGL-JANSSEN B et al.: Ligation of cell surface CD4 inhibits activation-induced death of human T lymphocytes at the level of Fas ligand expression. Immunol (1997) 159:5742–5749.
   Web of Science ®Google Scholar
• SANZENBACHER R, KABELITZ D, JANSSEN O: SLP-76 binding to p561ck: a role for SLP-76 in CD4-induced desensitization of the TCR/CD3 signaling complex. J. Immunol (1999) 163:3143–3152.
   PubMed Web of Science ®Google Scholar
• KAVURMA MM, KHACHIGIAN LM: Signaling and transcriptional control of Fas ligand gene expression. Cell Death Differ. (2003) 10:36–44.
   PubMed Web of Science ®Google Scholar
• •Review on FasL regulation at the level of transcription.
   Google Scholar
• BRUNNER T, KASIBHATLA S, PINKOSKI MJ et al.: Expression of Fas ligand in activated T cells is regulated by c-Myc. J. Biol. Chem. (2000) 275:9767–9772.
   PubMed Web of Science ®Google Scholar
• CHOW WA, FANG JJ, YEE JK: The IFN regulatory factor family participates in regulation of Fas ligand gene expression in T cells. J. Immunol (2000) 164:3512–3518.
   PubMed Web of Science ®Google Scholar
• KASIBHATLA S, GENESTIER L, GREEN DR: Regulation of fas-ligand expression during activation-induced cell death in T lymphocytes via nuclear factor kappaB. Biol. Chem. (1999) 274:987–992.
   Google Scholar
• LATINIS KM, NORIAN LA, ELIASON SL, KORETZKY GA: Two NFAT transcription factor binding sites participate in the regulation of CD95 (Fas) ligand expression in activated human T cells. J. Biol. Chem. (1997) 272:31427–31434.
   PubMedGoogle Scholar
• MITTELSTADT PR, ASHWELL JD: Cyclosporin A-sensitive transcription factor Egr-3 regulates Fas ligand expression. Ma. Cell Biol. (1998) 18:3744–3751.
   Web of Science ®Google Scholar
• MITTELSTADT PR, ASHWELL JD: Role of Egr-2 in up-regulation of Fas ligand in normal T cells and aberrant double-negative lpr and gld T cells. Biol. Chem. (1999) 274:3222–3227.
   Web of Science ®Google Scholar
• DZIALO-HATTON R, MILBRANDT J, HOCKETT RD Jr, WEAVER CT: Differential expression of Fas ligand in Thl and Th2 cells is regulated by early growth response gene and NF-AT family members. Immunol (2001) 166:4534–4542.
   Web of Science ®Google Scholar
• BRUNET A, BONNI A, ZIGMOND MJ et al.: Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Cell (1999) 96:857–868.
   PubMed Web of Science ®Google Scholar
• FARIS M, LATINIS KM, KEMPIAK SJ, KORETZKY GA, NEL A: Stress-induced Fas ligand expression in T cells is mediated through a MEK kinase 1-regulated response element in the Fas ligand promoter. Ma. Cell Biol. (1998) 18:5414–5424.
   Web of Science ®Google Scholar
• SCHNEIDER P, HOLLER N, BODMER JL et al.: Conversion of membrane-bound Fas(CD95) ligand to its soluble form is associated with downregulation of its proapoptotic, activity and loss of liver toxicity. J Exp. Med. (1998) 187:1205–1213.
   PubMed Web of Science ®Google Scholar
• TANAKA M, SUDA T, TAKAHASHI T, NAGATA S: Expression of the functional soluble form of human fas ligand in activated lymphocytes. EMBO J. (1995) 14:1129–1135.
   PubMed Web of Science ®Google Scholar
• TANAKA M, ITAI T, ADACHI M, NAGATA S: Downregulation of Fas ligand by shedding. Nat. Med. (1998) 4:31–36.
   PubMed Web of Science ®Google Scholar
• •The observations by Tanaka and co-workers (see also [60]) initiated the still ongoing discussion about shedding and the role of the soluble FasL.
   Google Scholar
• SUDA T, HASHIMOTO H, TANAKA M, OCHI T, NAGATA S: Membrane Fas ligand kills human peripheral blood T lymphocytes, and soluble Fas ligand blocks the killing. J. Exp. Med. (1997) 186:2045–2050.
   PubMed Web of Science ®Google Scholar
• •The authors hypothesize that oligomerisation of FasL is required for effective signalling through the Fas receptor. Thus, soluble FasL acts as an antagonist for the membrane molecule.
   Google Scholar
• HOLLER N, TARDIVEL A, KOVACSOVICS-BANKOWSKI M et al: Two adjacent trimeric Fas ligands are required for Fas signaling and formation of a death-inducing signaling complex. Mol. Cell Biol. (2003) 23:1428–1440.
   PubMed Web of Science ®Google Scholar
• MARTINEZ-LORENZO MJ, ALAVA MA, ANEL A, PINEIRO A, NAVAL J: Release of preformed Fas ligand in soluble form is the major factor for activation-induced death of Jurkat T cells. Immunology (1996) 89:511–517.
   PubMed Web of Science ®Google Scholar
• OTTONELLO L, TORTOLINA G, AMELOTTI M, DALLEGRI F: Soluble Fas ligand is chemotactic for human neutrophilic polymorphonuclear leukocytes. J. Immunol (1999) 162:3601-3606. SEINO K, IWABUCHI K, KAYAGAKI N et al: Chemotactic activity of soluble Fas ligand against phagocytes. J. Immunol (1998) 161:4484-4488. Describes chemotazis as another function of FasL.
   Google Scholar
• SHUDO K, KINOSHITA K, IMAMURA R et al: The membrane-bound but not the soluble form of human Fas ligand is responsible for its inflammatory activity. Eur. I Immunol (2001) 31:2504–2511.
   PubMed Web of Science ®Google Scholar
• VARGO-GOGOLA T, FINGLETON B, CRAWFORD HC, MATRISIAN LM: Matrilysin (matrix metalloproteinase-7) selects for apoptosis-resistant mammary cells in vivo. Cancer Res. (2002) 62:5559–5563.
   PubMed Web of Science ®Google Scholar
• VARGO-GOGOLA T, CRAWFORD HC, FINGLETON B, MATRISIAN LM: Identification of novel matrix metalloproteinase-7 (matrilysin) cleavage sites in murine and human Fas ligand. Arch. Biochem. Biophys. (2002) 408:155–161.
   PubMed Web of Science ®Google Scholar
• ROSENDAHL MS, KO SC, LONG DL et al: Identification and characterization of a pro-tumor necrosis factor-alpha-processing enzyme from the ADAM family of zinc metalloproteases. ./. Biol. Chem. (1997) 272:24588–24593.
   PubMed Web of Science ®Google Scholar
• POWELL WC, FINGLETON B, WILSON CL, BOOTHBY M, MATRISIAN LM: The metalloproteinase matrilysin proteolytically generates active soluble Fas ligand and potentiates epithelial cell apoptosis. Curr. Biol. (1999) 9:1441–1447.
   PubMed Web of Science ®Google Scholar
• •Matrilysin (MMP-7) is capable of cleaving FasL from the cell surface and has therefore been considered a target for therapy.
   Google Scholar
• STRAND S, VOLLMER P, VAN DEN ABEELEN L et al.: Cleavage of CD95 (APO-1, Fas) by matrilysin (MMP-7) induces apoptosis resistance in tumor cells. Oncogene. (2004) 23:3732–3736.
   Google Scholar
• CRAWFORD HC, SCOGGINS CR, WASHINGTON MK, MATRISIAN LM, LEACH SD: Matrix metalloproteinase-7 is expressed by pancreatic cancer precursors and regulates acinar-to-ductal metaplasia in exocrine pancreas. J Clin. Invest. (2002) 109:1437–1444.
   PubMed Web of Science ®Google Scholar
• TANAKA M, SUDA T, HAZE K et al: Fas ligand in human serum. Nat. Med. (1996) 2:317–322.
   PubMed Web of Science ®Google Scholar
• •Among the first reports on soluble FasL in sera of patients. Opened the field of defining FasL as a marker for disease progression.
   Google Scholar
• BOSSI G, STINCHCOMBE JC, PAGE LJ, GRIFFITHS GM: Sorting out the multiple roles of Fas ligand. Eur. J. Cell Biol. (2000) 79:539–543.
   PubMed Web of Science ®Google Scholar
• RUSSELL JH, LEY TJ: Lymphocyte-mediated cytotoxicity. Ann. Rev Immunol (2002) 20:323–370.
   PubMed Web of Science ®Google Scholar
• GRIFFITHS GM: Albinism and immunity: what's the link? Curr. Mol. Med. (2002) 2:479–483.
   Google Scholar
• CLARK R, GRIFFITHS GM: Lytic granules, secretory lysosomes and disease. Curr. Opin. Immunol (2003) 15:516–521.
   PubMed Web of Science ®Google Scholar
• STINCHCOMBE J, BOSSI G, GRIFFITHS GM: Linking albinism and immunity: the secrets of secretory lysosomes. Science (2004) 305:55–59.
   PubMed Web of Science ®Google Scholar
• LETOURNEUR F, KLAUSNER R D: A novel di-leucine motif and a tyrosine-based motif independently mediate lysosomal targeting and endocytosis of CD3 chains. Cell (1992) 69:1143–1157.
   PubMed Web of Science ®Google Scholar
• TROWBRIDGE IS, COLLAWN JF, HOPKINS CR: Signal-dependent membrane protein trafficking in the endocytic pathway. Ann. Rev. Cell Biol. (1993) 9:129–161.
   PubMedGoogle Scholar
• BLOTT EJ, BOSSI G, CLARK R, ZVELEBIL M, GRIFFITHS GM: Fas ligand is targeted to secretory lysosomes via a proline-rich domain in its cytoplasmic tail. I. Cell Sci. (2001) 114:2405–2416.
   PubMed Web of Science ®Google Scholar
• •This paper shows that the FasL PRD is required for sorting Fas ligand to the secretory lysosomes. It points to the functional relevance of the unique cytoplasmic tail of FasL for safe storage of a potentially dangerous molecule.
   Google Scholar
• HANE M, LOWIN B, PEITSCH M, BECKER K, TSCHOPP J: Interaction of peptides derived from the Fas ligand with the Fyn-SH3 domain. FEBS Lett. (1995) 373: 265–268.
   PubMed Web of Science ®Google Scholar
• •Identification of the Sit kinase p59fyn as a putative FasL interactor.
   Google Scholar
• GHADIMI MP, SANZENBACHER R, THIEDE B et al.: Identification of interaction partners of the cytosolic polyproline region of CD95 ligand (CD178). FEBS Lett. (2002) 519:50–58.
   PubMed Web of Science ®Google Scholar
• WENZEL J, SANZENBACHER R, GHADIMI M et al.: Multiple interactions of the cytosolic polyproline region of the CD95 ligand: hints for the reverse signal transduction capacity of a death factor. FEBS Lett. (2001) 509:255–262.
   PubMed Web of Science ®Google Scholar
• JANSSEN O, QIAN J, LINKERMANN A, KABELITZ D: CD95 Ligand - death factor and constimulatory molecule? Cell Death Differ. (2003) 10:1215–1225.
   Google Scholar
• LINKERMANN A, QIAN J, KABELITZ D, JANSSEN O: The Fas ligand as a cell death factor and signal transducer. Signal Transduction. (2003) 3:33–34.
   Google Scholar
• RIVERO-LEZCANO OM, MARCILLA A, SAMESHIMA JH, ROBBINS KC: Wiskott-Aldrich syndrome protein physically associates with Nck through Src homology 3 domains. Mol. Cell Biol. (1995) 15:5725–5731.
   PubMed Web of Science ®Google Scholar
• ANTON IM, LU W, MAYER BJ, RAMESH N, GEHA RS: The Wiskott-Aldrich syndrome protein-interacting protein (WIP) binds to the adaptor protein Nck. J Biol. Chem. (1998) 273:20992–20995.
   PubMedGoogle Scholar
• GILD, SCHAMEL WW, MONTOYA M, SANCHEZ-MADRID F, ALARCON B: Recruitment of Nck by CD3 epsilon reveals a ligand-induced conformational change essential for T cell receptor signaling and synapse formation. Cell (2002) 109:901–912.
   PubMed Web of Science ®Google Scholar
• •Nck as a link between the TCR and the actin cytoskeleton.
   Google Scholar
• LUSSIER G, LAROSE L: A casein kinase Iactivity is constitutively associated with Nck. .1 Biol. Chem. (1997) 272:2688–2694.
   PubMed Web of Science ®Google Scholar
• WATTS AD, HUNT NH, WANIGASEKARA Y et al.: A casein kinase I motif present in the cytoplasmic domain of members of the tumour necrosis factor ligand family is implicated in 'reverse signalling'. EMBO J. (1999) 18:2119–2126.
   PubMed Web of Science ®Google Scholar
• JANSSEN O, STOCKER A, SANZENBACHER R et al.: Differential regulation of activation-induced cell death in individual human T cell clones. Int. Arch. Allergy Immunol. (2000) 121:183–193.
   PubMed Web of Science ®Google Scholar
• SUZUKI I, FINK P J: Maximal proliferation of cytotoxic T lymphocytes requires reverse signaling through Fas ligand. J. Exp. Med. (1998) 187:123-128. •In vivo model indicating the reverse signalling capacity of FasL in cytotoxic T cells.
   Google Scholar
• DESBARATS J, DUKE RC, NEWELL MK: Newly discovered role for Fas ligand in the cell-cycle arrest of CD4+ cells. Nature. Med. (1998) 4:1377-1382.•In vivo model indicating the reverse signalling capacity of FasL in CD4-positive cells.
   Google Scholar
• SUZUKI I, FINK PJ: The dual functions of fas ligand in the regulation of peripheral CD8+ and CD4+ T cells. Proc. Nati Acad. Sci. USA (2000) 97:1707–1712.
   PubMed Web of Science ®Google Scholar
• BLOTT EJ, GRIFFITHS GM: Secretory lysosomes. Nat. Rev Mol. Cell Biol. (2002) 3:122–131.
   PubMed Web of Science ®Google Scholar
• STINCHCOMBE JC, BOSSI G, BOOTH S, GRIFFITHS GM: The immunological synapse of CTL contains a secretory domain and membrane bridges. Immunio, (2001) 15:751–761.
   PubMed Web of Science ®Google Scholar
• LETTAU M, QIAN J, KABELITZ D, JANSSEN O: Activation-dependent FasL expression in T lymphocytes and Natural Killer cells. Signal Transduction (2004) 4:In press.
   Google Scholar
• BOURSALIAN TE, FINK PJ: Mutation in fas ligand impairs maturation of thymocytes bearing moderate affinity T cell receptors. Exp. Med. (2003) 198:349–360.
   PubMed Web of Science ®Google Scholar
• TRAUTH BC, KLAS C, PETERS AM et al.: Monoclonal antibody-mediated tumor regression by induction of apoptosis. Science (1989) 245:301–305.
   PubMed Web of Science ®Google Scholar
• OGASAWARA J, WATANABE-FUKUNAGA R, ADACHI M et al.: Lethal effect of the anti-Fas antibody in mice. Nature (1993) 364:806–809.
   PubMed Web of Science ®Google Scholar
• NAKAMOTO Y, KANEKO S, FAN H et al.: Prevention of hepatocellular carcinoma development associated with chronic hepatitis by anti-fas ligand antibody therapy. J. Exp. Med. (2002) 196:1105–1111.
   PubMed Web of Science ®Google Scholar
• DEMJEN D, KLUSSMANN S, KLEBER S et al.: Neutralization of CD95 ligand promotes regeneration and functional recovery after spinal cord injury. Nat. Med. (2004) 10:389–395.
   PubMed Web of Science ®Google Scholar
• GUERY L, BATTEUX F, BESSIS N et al.: Expression of Fas ligand improves the effect of IL-4 in collagen-induced arthritis. Eur. Immunol. (2000) 30:308–315.
   PubMed Web of Science ®Google Scholar
• KIM SH, KIM S, OLIGINO TJ, ROBBINS PD: Effective treatment of established mouse collagen-induced arthritis by systemic administration of dendritic cells genetically modified to express FasL. Mol. Ther. (2002) 6:584–590.
   PubMed Web of Science ®Google Scholar
• MODIANO JF, SUN J, LANG J et al.: Fas ligand-dependent suppression of autoimmunity via recruitment and subsequent termination of activated T cells. Clin. Immunol. (2004) 112:54–65.
   PubMed Web of Science ®Google Scholar
• MAY, LIU H, TU-RAPP H et al: Fas ligation on macrophages enhances IL-1R1-Toll-like receptor 4 signaling and promotes chronic inflammation. Nat. Immunol. (2004) 5:380–387.
   PubMed Web of Science ®Google Scholar
• CHUANG YH, FU CL, LO YC, CHIANG BL: Adenovirus expressing Fas ligand gene decreases airway hyper-responsiveness and eosinophilia in a murine model of asthma. Gene Ther. (2004) 11:1497–1505.
   PubMed Web of Science ®Google Scholar
• JIANG C, YANG YE CHENG SH: Fas ligand gene therapy for vascular intimal hyperplasia. Curr. Gene Ther. (2004) 4:33–39.
   PubMed Web of Science ®Google Scholar
• NORRIS JS, HYER ML, VOELKEL-JOHNSON C et al.: The use of Fas Ligand, TRAIL and Bax in gene therapy of prostate cancer. Curr. Gene Ther. (2001) 1:123–136.
   PubMedGoogle Scholar
• SUDARSHAN S, HOLMAN DH, HYER ML et al.: hi vitro efficacy of Fas ligand gene therapy for the treatment of bladder cancer. Cancer Gene Ther. (2004).
   Google Scholar
• AMBAR BB, FRET K, MALIPIERO U et al.: Treatment of experimental glioma by administration of adenoviral vectors expressing Fas ligand. Hum. Gene Ther. (1999) 10:1641–1648.
   PubMed Web of Science ®Google Scholar
• RUBINCHIK S, YU H, WORARATANADHARM J et al.: Enhanced apoptosis of glioma cell lines is achieved by co-delivering FasL-GFP and TRAIL with a complex Ad5 vector. Cancer Gene Ther. (2003) 10:814–822.
   PubMed Web of Science ®Google Scholar
• ARAI H, GORDON D, NABEL EG, NABEL GJ: Gene transfer of Fas ligand induces tumor regression in vivo. Proc. Natl. Acad. Sci. USA (1997) 94:13862–13867.
   PubMed Web of Science ®Google Scholar
• LI-WEBER M, WEIGAND MA, GIAISI M et al.: Vitamin E inhibits CD95 ligand expression and protects T cells from activation-induced cell death. J. Clin. Invest (2002) 110:681–690.
   PubMed Web of Science ®Google Scholar
• LI-WEBER M, GIAISI M, BAUMANN S, TREIBER MK, KRAMMER PH: The anti-inflammatory sesquiterpene lactone parthenolide suppresses CD95-mediated activation-induced cell death in T-cells. Cell Death Differ. (2002) 9:1256–1265.
   PubMed Web of Science ®Google Scholar