Document Detail


Leflunomide suppresses TNF-induced cellular responses: effects on NF-kappa B, activator protein-1, c-Jun N-terminal protein kinase, and apoptosis.
MedLine Citation:
PMID:  11067959     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Leflunomide is a pyrimidine biosynthesis inhibitor that has recently been approved for treatment of rheumatoid arthritis. However, the mechanism of leflunomide's antiarthritis activity and is not fully understood. The critical role that TNF plays in rheumatoid arthritis led us to postulate that leflunomide blocks TNF signaling. Previously, we have demonstrated that leflunomide inhibits TNF-induced NF-kappaB activation by suppressing I-kappaBalpha (inhibitory subunit of NF-kappaB) degradation. We in this study show that leflunomide also blocks NF-kappaB reporter gene expression induced by TNFR1, TNFR-associated factor 2, and NF-kappaB-inducing kinase (NIK), but not that activated by the p65 subunit of NF-kappaB, suggesting that leflunomide acts downstream of NIK. Leflunomide suppressed TNF-induced phosphorylation of I-kappaBalpha, as well as activation of I-kappaBalpha kinase-beta located downstream to NIK. Leflunomide also inhibited TNF-induced activation of AP-1 and the c-Jun N-terminal protein kinase activation. TNF-mediated cytotoxicity and caspase-induced poly(ADP-ribose) polymerase cleavage were also completely abrogated by treatment of Jurkat T cells with leflunomide. Leflunomide suppressed TNF-induced reactive oxygen intermediate generation and lipid peroxidation, which may explain most of its effects on TNF signaling. The suppressive effects of leflunomide on TNF signaling were completely reversible by uridine, indicating a critical role for pyrimidine biosynthesis in TNF-mediated cellular responses. Overall, our results suggest that suppression of TNF signaling is one of the possible mechanisms for inhibitory activity of leflunomide against rheumatoid arthritis.
Authors:
S K Manna; A Mukhopadhyay; B B Aggarwal
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  165     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2000 Nov 
Date Detail:
Created Date:  2000-11-21     Completed Date:  2000-12-22     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  5962-9     Citation Subset:  AIM; IM    
Affiliation:
Cytokine Research Laboratory, Department of Bioimmunotherapy, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*
Caspases / antagonists & inhibitors,  metabolism
Cells, Cultured
Cytotoxicity, Immunologic / drug effects
DNA-Binding Proteins / antagonists & inhibitors,  metabolism
Enzyme Activation / drug effects,  immunology
Gene Expression Regulation / drug effects,  immunology
Genes, Reporter / immunology
Growth Inhibitors / pharmacology*
Hela Cells
Humans
I-kappa B Kinase
I-kappa B Proteins*
Immunosuppressive Agents / antagonists & inhibitors,  pharmacology*
Isoxazoles / antagonists & inhibitors,  pharmacology*
JNK Mitogen-Activated Protein Kinases
Jurkat Cells
Lipid Peroxidation / drug effects,  immunology
Mitogen-Activated Protein Kinases / antagonists & inhibitors*,  metabolism
NF-kappa B / antagonists & inhibitors*,  biosynthesis,  genetics,  metabolism
Phosphorylation
Protein-Serine-Threonine Kinases / antagonists & inhibitors,  metabolism
Reactive Oxygen Species / immunology,  metabolism
Receptors, Tumor Necrosis Factor / metabolism
Signal Transduction / drug effects,  immunology
Transcription Factor AP-1 / antagonists & inhibitors*,  metabolism
Tumor Necrosis Factor-alpha / antagonists & inhibitors,  physiology*
Uridine / pharmacology
Chemical
Reg. No./Substance:
0/DNA-Binding Proteins; 0/Growth Inhibitors; 0/I-kappa B Proteins; 0/Immunosuppressive Agents; 0/Isoxazoles; 0/NF-kappa B; 0/Reactive Oxygen Species; 0/Receptors, Tumor Necrosis Factor; 0/Transcription Factor AP-1; 0/Tumor Necrosis Factor-alpha; 139874-52-5/NF-kappaB inhibitor alpha; 58-96-8/Uridine; 75706-12-6/leflunomide; EC 2.7.1.-/IKBKE protein, human; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.10/CHUK protein, human; EC 2.7.11.10/I-kappa B Kinase; EC 2.7.11.10/IKBKB protein, human; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 3.4.22.-/Caspases

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