Cytokines and hormones with anti inflammatory effects: new tools for therapeutic intervention

被引：4

作者：

Baud, L

Fouqueray, B

Bellocq, A

机构：

[1] Hop Tenon, Serv Explorat Fonct Multidisciplinaires, F-75020 Paris, France

[2] Hop Tenon, INSERM, U489, F-75020 Paris, France

来源：

CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION | 2001年 / 10卷 / 01期

关键词：

D O I：

10.1097/00041552-200101000-00008

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

The inflammation that is involved in the development of glomerulonephritis is tightly regulated by the expression of antiinflammatory factors. These include circulating hormones, such as glucocorticoids, and mediators that are produced by intrinsic cells and infiltrating leucocytes. The present review focuses on these anti-inflammatory factors, summarizing in particular their activities in existing models of glomerulonephritis. In addition, experimental evidence is presented that anti-inflammatory mediators are able to increase glucocorticoid binding or signalling in target cells. These data help to explain the in-vivo efficacy of anti-inflammatory mediators, and offer a promising new avenue for therapeutic intervention. Curr Opin Nephrol Hypertens 10:49-54. (C) 2001 Lippincott Williams & Wilkins.

引用

收藏

页码：49 / 54

页数：6

相关论文

共 50 条

[31] Endogenous glucocorticoids modulate experimental anti-glomerular basement membrane glomerulonephritis [J].

Leech, M ;

Huang, XR ;

Morand, EF ;

Holdsworth, SR .

CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2000, 119 (01) :161-168

[32] Molecular control of immune/inflammatory responses: Interactions between nuclear factor-κB and steroid receptor-signaling pathways [J].

McKay, LI ;

Cidlowski, JA .

ENDOCRINE REVIEWS, 1999, 20 (04) :435-459

[33] In situ upregulation of IL-10 reflects the activity of human glomerulonephritides [J].

Niemir, ZI ;

Ondracek, M ;

Dworacki, G ;

Stein, H ;

Waldherr, R ;

Ritz, E ;

Otto, HF .

AMERICAN JOURNAL OF KIDNEY DISEASES, 1998, 32 (01) :80-92

[34]

PELTIER J, IN PRESS NEPHROL DIA

[35] Specificity, diversity, and regulation in TGF-β superfamily signaling [J].

Piek, E ;

Heldin, CH ;

Ten Dijke, P .

FASEB JOURNAL, 1999, 13 (15) :2105-2124

[36] Corticosteroids in IgA nephropathy: a randomised controlled trial [J].

Pozzi, C ;

Bolasco, PG ;

Fogazzi, GB ;

Andrulli, S ;

Altieri, P ;

Ponticelli, C ;

Locatelli, F .

LANCET, 1999, 353 (9156) :883-887

[37]

Ripley BJM, 1999, IMMUNOLOGY, V97, P226

[38] Early treatment with corticosteroids ameliorates proteinuria, proliferative lesions, and mesangial phenotypic modulation in adult diffuse proliferative IgA nephropathy [J].

Shoji, T ;

Nakanishi, I ;

Suzuki, A ;

Hayashi, T ;

Togawa, M ;

Okada, N ;

Imai, E ;

Hori, M ;

Tsubakihara, Y .

AMERICAN JOURNAL OF KIDNEY DISEASES, 2000, 35 (02) :194-201

[39] TGF-β1 stimulates expression of the aromatase (CYP19) gene in human osteoblast-like cells and THP-1 cells [J].

Shozu, M ;

Zhao, Y ;

Simpson, ER .

MOLECULAR AND CELLULAR ENDOCRINOLOGY, 2000, 160 (1-2) :123-133

[40] Glucocorticoid receptor inhibits transforming growth factor-β signaling by directly targeting the transcriptional activation function of Smad3 [J].

Song, CZ ;

Tian, X ;

Gelehrter, TD .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (21) :11776-11781

← 1 2 3 4 5 →