The importance of glucocorticoid receptors in systemic lupus erythaematosus. A systematic review

被引:31
作者
Bazso, Anna [1 ]
Szappanos, Agnes [1 ]
Patocs, Attila [2 ]
Poor, Gyula [1 ,4 ]
Shoenfeld, Yehuda [3 ]
Kiss, Emese [1 ,4 ]
机构
[1] Natl Inst Rheumatism & Physiotherapy, Budapest, Hungary
[2] Semmelweis Univ, Dept Med 2, H-1085 Budapest, Hungary
[3] Tel Aviv Univ, Zabludowicz Ctr Autoimmune Dis, IL-69978 Tel Aviv, Israel
[4] Semmelweis Univ, Dept Med 3, H-1085 Budapest, Hungary
关键词
SLE; Glucocorticoids; Genetic polymorphisms; Glucocorticoid receptors; MOLECULAR-MECHANISMS; DISEASE-ACTIVITY; INHIBITION; EXPRESSION; PATHWAY; ALPHA; AXIS;
D O I
10.1016/j.autrev.2014.12.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
The therapeutic management of systemic lupus erythaematosus (SLE) is still a great debate. Despite the latest innovation agents or developing trials, there is not an integrated and common approach for treating SLE. For decades, natural and synthetic glucocorticoids (GCs) have been the first and most frequently used immune suppressive agents in SLE. Therefore, GCs are the most important therapy in SLE in daily routine, however the response to GCs differs widely and long-term therapy is associated with side-effects. Still now, clinicians and physicians are unable to predict the exact and ideal dose and term of therapy for patients suffering from various symptoms and degree of disease activity of SLE. The biological mechanism of GCs is regulated through activation of glucocorticoid receptors (GRs). There are two major isoforms of GRs: GR alpha and GR beta; however, the GR alpha is the predominant one which binds steroids and activates target genes. In the present review, we summarise the anti-inflammatory and immune suppressive effects of GCs via GRs to regulate the target genes. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:349 / 351
页数:3
相关论文
共 39 条
[1]
The importance of assessing medication exposure to the definition of refractory disease in systemic lupus erythematosus [J].
Arnaud, Laurent ;
Zahr, Noel ;
Costedoat-Chalumeau, Nathalie ;
Amoura, Zahir .
AUTOIMMUNITY REVIEWS, 2011, 10 (11) :674-678
[2]
IMMUNOSUPPRESSION BY GLUCOCORTICOIDS - INHIBITION OF NF-KAPPA-B ACTIVITY THROUGH INDUCTION OF I-KAPPA-B SYNTHESIS [J].
AUPHAN, N ;
DIDONATO, JA ;
ROSETTE, C ;
HELMBERG, A ;
KARIN, M .
SCIENCE, 1995, 270 (5234) :286-290
[3]
Besedovsky HO, 2000, Z RHEUMATOL, V59, P26, DOI 10.1007/s003930070014
[4]
Identification of target genes involved in the antiproliferative effect of glucocorticoids reveals a role for nuclear factor-κB repression [J].
Bladh, LG ;
Lidén, J ;
Pazirandeh, A ;
Rafter, I ;
Dahlman-Wright, K ;
Nilsson, S ;
Okret, S .
MOLECULAR ENDOCRINOLOGY, 2005, 19 (03) :632-643
[5]
The geoepidemiology of systemic lupus erythematosus [J].
Borchers, Andrea T. ;
Naguwa, Stanley M. ;
Shoenfeld, Yehuda ;
Gershwin, M. Eric .
AUTOIMMUNITY REVIEWS, 2010, 9 (05) :A277-A287
[6]
Glucocorticoid receptor-JNK interaction mediates inhibition of the JNK pathway by glucocorticoids [J].
Bruna, A ;
Nicolàs, M ;
Muñoz, A ;
Kyriakis, JM ;
Caelles, C .
EMBO JOURNAL, 2003, 22 (22) :6035-6044
[7]
Ectoderm-targeted overexpression of the glucocorticoid receptor induces hypohidrotic ectodermal dysplasia [J].
Cascallana, JL ;
Bravo, A ;
Donet, E ;
Leis, H ;
Lara, MF ;
Paramio, JM ;
Jorcano, JL ;
Pérez, P .
ENDOCRINOLOGY, 2005, 146 (06) :2629-2638
[8]
Quantitation of glucocorticoid receptor alpha and NF-κB pathway mRNA and its correlation with disease activity in rheumatoid arthritis patients [J].
Cavalcante, L. O. ;
Melo, M. R. ;
Dinis, V. G. ;
Castro, R. B. ;
Souza, B. D. B. ;
Longui, C. A. .
GENETICS AND MOLECULAR RESEARCH, 2010, 9 (04) :2300-2310
[9]
Estrogens and autoimmune diseases [J].
Cutolo, Maurizio ;
Capellino, Silvia ;
Sulli, Alberto ;
Serioli, Bruno ;
Secchi, Maria Elena ;
Villaggio, Barbara ;
Straubb, Rawer H. .
ESTROGENS AND HUMAN DISEASES, 2006, 1089 :538-547
[10]
Pharmacokinetics and pharmacodynamics of systemically administered glucocorticoids [J].
Czock, D ;
Keller, F ;
Rasche, FM ;
Häussler, U .
CLINICAL PHARMACOKINETICS, 2005, 44 (01) :61-98