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*
Department of Microbiology, and
The Arthritis Center, Department of Medicine, School of Medicine, Boston University, Boston, MA 02118; and
The Schepens Eye Research Institute, Boston, MA 02114
Fas ligand (FasL) is a potent proapoptotic type-II transmembrane
protein that can cause cell death in Fas+ target
populations. Despite the presumed "silent" nature of apoptotic cell
death, forced expression of FasL can induce a dramatic inflammatory
response. To elucidate the in vivo mechanism(s) linking FasL and
inflammation, we used a membrane-bound cell-free form of FasL
(mFasL-vesicle preparation (VP)). We found that i.p. injection of
FasL-microvesicles led to the rapid activation and subsequent demise of
Mac1high resident peritoneal macrophages. Apoptosis of
Mac1high peritoneal macrophages was observed within
0.5 h of mFasL-VP injection and correlated with the detection of
increased macrophage inflammatory protein (MIP)-2 levels in peritoneal
lavage fluid as well as induced RNA expression of IL-1
, MIP-2,
MIP-1
, and MIP-1. In vitro culture of purified peritoneal
populations identified Mac1high cells as the major
cytokine/chemokine producers in response to mFasL-VP. Purified
Mac1high cells exposed to FasL could restore the ability of
Fas-deficient mice to mount an inflammatory response. Our data
demonstrate that the FasL-mediated inflammatory response starts with
the production of proinflammatory mediators by preapoptotic resident
tissue macrophages and suggest a general mechanism responsible for
neutrophil inflammation seen in cases of FasL-expressing
allografts.
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W.-S. Hor, W.-L. Huang, Y.-S. Lin, and B.-C. Yang Cross-talk between tumor cells and neutrophils through the Fas (APO-1, CD95)/FasL system: human glioma cells enhance cell viability and stimulate cytokine production in neutrophils J. Leukoc. Biol., March 1, 2003; 73(3): 363 - 368. [Abstract] [Full Text] [PDF]
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K. Roessner, J. Wolfe, C. Shi, L. H. Sigal, S. Huber, and R. C. Budd High Expression of Fas Ligand by Synovial Fluid-Derived {gamma}{delta} T Cells in Lyme Arthritis J. Immunol., March 1, 2003; 170(5): 2702 - 2710. [Abstract] [Full Text] [PDF]
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S. Xiao, S. Jodo, S.-s. J. Sung, A. Marshak-Rothstein, and S.-T. Ju A Novel Signaling Mechanism for Soluble CD95 Ligand. SYNERGY WITH ANTI-CD95 MONOCLONAL ANTIBODIES FOR APOPTOSIS AND NF-kappa B NUCLEAR TRANSLOCATION J. Biol. Chem., December 20, 2002; 277(52): 50907 - 50913. [Abstract] [Full Text] [PDF]
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M. S. Gregory, A. C. Repp, A. M. Holhbaum, R. R. Saff, A. Marshak-Rothstein, and B. R. Ksander Membrane Fas Ligand Activates Innate Immunity and Terminates Ocular Immune Privilege J. Immunol., September 1, 2002; 169(5): 2727 - 2735. [Abstract] [Full Text] [PDF]
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 V. M. Borges, M. F. Lopes, H. Falcao, J. H. Leite-Junior, P. R. M. Rocco, W. F. Davidson, R. Linden, W. A. Zin, and G. A. DosReis Apoptosis Underlies Immunopathogenic Mechanisms in Acute Silicosis Am. J. Respir. Cell Mol. Biol., July 1, 2002; 27(1): 78 - 84. [Abstract] [Full Text] [PDF]
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F. H. Igney and P. H. Krammer Immune escape of tumors: apoptosis resistance and tumor counterattack J. Leukoc. Biol., June 1, 2002; 71(6): 907 - 920. [Abstract] [Full Text] [PDF]
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