Type I IFN and TNFα cross-regulation in immune-mediated inflammatory disease: basic concepts and clinical relevance

被引:89
作者
Cantaert, Tineke [1 ]
Baeten, Dominique [1 ]
Tak, Paul P. [1 ]
van Baarsen, Lisa G. M. [1 ]
机构
[1] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands
关键词
TUMOR-NECROSIS-FACTOR; SYSTEMIC-LUPUS-ERYTHEMATOSUS; COLLAGEN-INDUCED ARTHRITIS; INTERFERON-BETA TREATMENT; PRIMARY SJOGRENS-SYNDROME; PERIPHERAL-BLOOD CELLS; JUVENILE DERMATOMYOSITIS; HUMORAL AUTOIMMUNITY; MULTIPLE-SCLEROSIS; GENE-EXPRESSION;
D O I
10.1186/ar3150
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
A cross-regulation between type I IFN and TNF alpha has been proposed recently, where both cytokines are hypothesized to counteract each other. According to this model, different autoimmune diseases can be viewed as disequilibrium between both cytokines. As this model may have important clinical implications, the present review summarizes and discusses the currently available clinical evidence arguing for or against the proposed cross-regulation between TNF alpha and type I IFN. In addition, we review how this cross-regulation works at the cellular and molecular levels. Finally, we discuss the clinical relevance of this proposed cross-regulation for biological therapies such as type I IFN or anti-TNF alpha treatment.
引用
收藏
页数:10
相关论文
共 68 条
[1]   Mesenchymal cell targeting by TNF as a common pathogenic principle in chronic inflammatory joint and intestinal diseases [J].
Armaka, Maria ;
Apostolaki, Maria ;
Jacques, Peggy ;
Kontoyiannis, Dimitris L. ;
Elewaut, Dirk ;
Kollias, George .
JOURNAL OF EXPERIMENTAL MEDICINE, 2008, 205 (02) :331-337
[2]   Type I interferon in systemic lupus erythematosus and other autoimmune diseases [J].
Banchereau, Jacques ;
Pascual, Virginia .
IMMUNITY, 2006, 25 (03) :383-392
[3]   Activation of the type I interferon system in primary Sjogren's syndrome -: A possible etiopathogenic mechanism [J].
Båve, U ;
Nordmark, G ;
Lövgren, T ;
Rönnelid, J ;
Cajander, S ;
Eloranta, ML ;
Alm, GV ;
Rönnblom, L .
ARTHRITIS AND RHEUMATISM, 2005, 52 (04) :1185-1195
[4]   Interferon and granulopoiesis signatures in systemic lupus erythematosus blood [J].
Bennett, L ;
Palucka, AK ;
Arce, E ;
Cantrell, V ;
Borvak, J ;
Banchereau, J ;
Pascual, V .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (06) :711-723
[5]   Interferon-beta(1b) treatment decreases tumor necrosis factor-alpha and increases interleukin-6 production in multiple sclerosis [J].
Brod, SA ;
Marshall, GD ;
Henninger, EM ;
Sriram, S ;
Khan, M ;
Wolinsky, JS .
NEUROLOGY, 1996, 46 (06) :1633-1638
[6]   Exposure to nuclear antigens contributes to the induction of humoral autoimmunity during tumour necrosis factor alpha blockade [J].
Cantaert, T. ;
De Rycke, L. ;
Mavragani, C. P. ;
Wijbrandts, C. A. ;
Niewold, T. B. ;
Niers, T. ;
Vandooren, B. ;
Veys, E. M. ;
Richel, D. ;
Tak, P. P. ;
Crow, M. K. ;
Baeten, D. .
ANNALS OF THE RHEUMATIC DISEASES, 2009, 68 (06) :1022-1029
[7]   Type I interferons have no major influence on humoral autoimmunity in rheumatoid arthritis [J].
Cantaert, Tineke ;
van Baarsen, Lisa G. ;
Wijbrandts, Carla A. ;
Thurlings, Rogier M. ;
van de Sande, Marleen G. ;
Bos, Carina ;
van der Pouw, Tineke Kraan ;
Verweij, Cor L. ;
Tak, Paul P. ;
Baeten, Dominique L. .
RHEUMATOLOGY, 2010, 49 (01) :156-166
[8]  
Coclet-Ninin J, 1997, EUR CYTOKINE NETW, V8, P345
[9]   A type I interferon signature in monocytes is associated with poor response to interferon-β in multiple sclerosis [J].
Comabella, M. ;
Luenemann, J. D. ;
Rio, J. ;
Sanchez, A. ;
Lopez, C. ;
Julia, E. ;
Fernandez, M. ;
Nonell, L. ;
Camina-Tato, M. ;
Deisenhammer, F. ;
Caballero, E. ;
Tortola, M. T. ;
Prinz, M. ;
Montalban, X. ;
Martin, R. .
BRAIN, 2009, 132 :3353-3365
[10]   Synergistic benefit in inflammatory arthritis by targeting IκB kinase ε and interferon β [J].
Corr, M. ;
Boyle, D. L. ;
Ronacher, L. ;
Flores, N. ;
Firestein, G. S. .
ANNALS OF THE RHEUMATIC DISEASES, 2009, 68 (02) :257-263