Abstract
As highlighted in the previous chapters, the interaction of Fas with Fas Ligand (FasL) affects many different aspects related to activation and apoptosis of Fas-expressing immune and tumor cells. Over the past five years we have learned, however, that FasL also acts as a costimulatory or accessory molecule for T cell activation. In the following chapter, we summarize what is known about FasL as a modulator of thymocyte development and selection or a regulator of mature T cell activation and effector function. Since to date almost no data are available on how a putative T cell receptor (TCR) /CD3-FasL crosstalk biochemically might work, we discuss ideas and hypotheses about the orchestration of retrograde signaling events also in the context of what is known from other members of the TNF family.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Suzuki I, Fink PJ. Maximal proliferation of cytotoxic T lymphocytes requires reverse signaling through Fas ligand. J Exp Med 1998; 187(1):123–128.
Desbarats J, Duke RC, Newell MK. Newly discovered role for Fas ligand in the cell-cycle arrest of CD4+ T cells. Nat Med 1998; 4(12):1377–1382.
Suzuki I, Fink PJ. The dual functions of fas ligand in the regulation of peripheral CD8+ and CD4+ T cells. Proc Natl Acad Sci USA 2000; 97(4):1707–1712.
Suzuki I, Martin S, Boursalian TE et al. Fas ligand costimulates the in vivo proliferation of CD8+ T cells. J Immunol 2000; 165(10):5537–5543.
Brunner T, Yoo NJ, Griffith TS et al. Regulation of CD 95 ligand expression: A key element in immune regulation? Behring Inst Mitt 1996; 97:161–174.
French LE, Hahne M, Viard I et al. Fas and Fas ligand in embryos and adult mice: Ligand expression in several immune-privileged tissues and coexpression in adult tissues characterized by apoptotic cell turnover. J Cell Biol 1996; 133(2):335–343.
Adachi M, Suematsu S, Suda T et al. Enhanced and accelerated lymphoproliferation in Fas-null mice. Proc Natl Acad Sci USA 1996; 93(5):2131–2136.
Sidman CL, Marshall JD, Von Boehmer H. Transgenic T cell receptor interactions in the lymphoproliferative and autoimmune syndromes of lpr and gld mutant mice. Eur J Immunol 1992; 22(2):499–504.
Singer GG, Abbas AK. The fas antigen is involved in peripheral but not thymic deletion of T lymphocytes in T cell receptor transgenic mice. Immunity 1994; 1(5):365–371.
Kishimoto H, Surh CD, Sprent J. A role for Fas in negative selection of thymocytes in vivo. J Exp Med 1998; 187(9):1427–1438.
Sprent J, Kishimoto H. The thymus and central tolerance. Philos Trans R Soc Lond B Biol Sci 2001; 356(1409):609–616.
Singer A. New perspectives on a developmental dilemma: The kinetic signaling model and the importance of signal duration for the CD4/CD8 lineage decision. Curr Opin Immunol 2002; 14(2):207–215.
Boursalian TE, Fink PJ. Mutation in fas ligand impairs maturation of thymocytes bearing moderate affinity T cell receptors. J Exp Med 2003; 198(2):349–360.
Janssen O, Qian J, Linkermann A et al. CD 95 ligand-death factor and costimulatory molecule? Cell Death Differ 2003; 10(11):1215–1225.
Hane M, Lowin B, Peitsch M et al. Interaction of peptides derived from the Fas ligand with the Fyn-SH3 domain. FEBS Lett 1995; 373(3):265–268.
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(2):255–262.
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(1–3):50–58.
Lussier G, Larose L. A casein kinase I activity is constitutively associated with Nck. J Biol Chem 1997; 272(5):2688–2694.
Linkermann A, Qian J, Kabelitz D et al. The Fas Ligand as a death factor and signal transducer? Signal Transduction 2003; 3(1–2):33–46.
Linkermann A, Qian J, Janssen O. Slowly getting a clue on CD95 ligand biology. Biochem Pharmacol 2003; 66(8):1417–1426.
Locksley RM, Killeen N, Lenardo MJ. The TNF and TNF receptor superfamilies: Integrating mammalian biology. Cell 2001; 104(4):487–501.
Lens SM, Drillenburg P, den Drijver BF et al. Aberrant expression and reverse signalling of CD70 on malignant B cells. Br J Haematol 1999; 106(2):491–503.
Cerutti A, Schaffer A, Goodwin RG et al. Engagement of CD153 (CD30 ligand) by CD30+ T cells inhibits class switch DNA recombination and antibody production in human IgD+ IgM+ B cells. J Immunol 2000; 165(2):786–794.
Wiley SR, Goodwin RG, Smith CA. Reverse signaling via CD30 ligand. J Immunol 1996; 157(8):3635–3639.
van Essen D, Kikutani H, Gray D. CD40 ligand-transduced costimulation of T cells in the development of helper function. Nature 1995; 378(6557):620–623.
Cayabyab M, Phillips JH, Lanier LL. CD40 preferentially costimulates activation of CD4+ T lymphocytes. J Immunol 1994; 152(4):1523–1531.
Miyashita T, McIlraith MJ, Grammer AC et al. Bidirectional regulation of human B cell responses by CD40-CD40 ligand interactions. J Immunol 1997; 158(10):4620–4633.
Blair PJ, Riley JL, Harlan DM et al. CD40 ligand (CD154) triggers a short-term CD4(+) T cell activation response that results in secretion of immunomodulatory cytokines and apoptosis. J Exp Med 2000; 191(4):651–660.
Langstein J, Michel J, Fritsche J et al. CD137 (ILA/4-1BB), a member of the TNF receptor family, induces monocyte activation via bidirectional signaling. J Immunol 1998; 160(5):2488–2494.
Langstein J, Michel J, Schwarz H. CD137 induces proliferation and endomitosis in monocytes. Blood 1999; 94(9):3161–3168.
Stuber E, Neurath M, Calderhead D et al. Cross-linking of OX40 ligand, a member of the TNF/NGF cytokine family, induces proliferation and differentiation in murine splenic B cells. Immunity 1995; 2(5):507–521.
Chen NJ, Huang MW, Hsieh SL. Enhanced secretion of IFN-gamma by activated Th1 cells occurs via reverse signaling through TNF-related activation-induced cytokine. J Immunol 2001; 166(1):270–276.
Scheu S, Alferink J, Potzel T et al. Targeted disruption of LIGHT causes defects in costimulatory T cell activation and reveals cooperation with lymphotoxin beta in mesenteric lymph node genesis. J Exp Med 2002; 195(12):1613–1624.
Shaikh RB, Santee S, Granger SW et al. Constitutive expression of LIGHT on T cells leads to lymphocyte activation, inflammation, and tissue destruction. J Immunol 2001; 167(11):6330–6337.
Morel Y, Truneh A, Sweet RW et al. The TNF superfamily members LIGHT and CD154 (CD40 ligand) costimulate induction of dendritic cell maturation and elicit specific CTL activity. J Immunol 2001; 167(5):2479–2486.
Eissner G, Kirchner S, Lindner H et al. Reverse signaling through transmembrane TNF confers resistance to lipopolysaccharide in human monocytes and macrophages. J Immunol 2000; 164(12):6193–6198.
Chou AH, Tsai HF, Lin LL et al. Enhanced proliferation and increased IFN-gamma production in T cells by signal transduced through TNF-related apoptosis-inducing ligand. J Immunol 2001; 167(3):1347–1352.
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 signaling’. EMBO J 1999; 18(8):2119–2126.
Author information
Authors and Affiliations
Rights and permissions
Copyright information
© 2006 Landes Bioscience and Springer Science+Business Media
About this chapter
Cite this chapter
Linkermann, A., Qian, J., Janssen, O. (2006). Retrograde Fas Ligand Signaling. In: Fas Signaling. Medical Intelligence Unit. Springer, Boston, MA. https://doi.org/10.1007/0-387-34573-6_7
Download citation
DOI: https://doi.org/10.1007/0-387-34573-6_7
Publisher Name: Springer, Boston, MA
Print ISBN: 978-0-387-32172-1
Online ISBN: 978-0-387-34573-4
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)