The immunopharmacological properties of transforming growth factor beta

被引:11
作者
Le, YY [1 ]
Yu, XJ
Ruan, LF
Wang, OM
Qi, DF
Zhu, JJ
Lu, XF
Kong, Y
Cai, K
Pang, SS
Shi, XL
Wang, JM
机构
[1] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Lab Immunol & Inflammatory Dis, Shanghai 200031, Peoples R China
[2] Chinese Acad Sci, Grad Sch, Shanghai 200031, Peoples R China
[3] NCI, Mol Immunoregulat Lab, Canc Res Ctr, Frederick, MD 21702 USA
关键词
transforming growth factor beta; inflammation; Alzheimer's disease;
D O I
10.1016/j.intimp.2005.07.006
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Transforming growth factor-beta (TGF-beta) family members are multifunctional molecules, which play pivotal roles in regulating cell proliferation, differentiation, migration, development, tissue remodeling and repair. These events are closely associated with host immune responses and inflammation. Despite some controversies on their function in controlling dendritic and T regulatory cell development and activity, the importance of TGF-beta s in the progress of autoimmunity and inflammatory diseases has been well appreciated and new aspects of their contribution continue to be recognized. Since one of the major biological properties of TGF-beta s is its capacity to potently suppress immune responses, they are considered as candidates for the development of therapeutic agents to fend off undesirable damage associated with immune and inflammatory conditions. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:1771 / 1782
页数:12
相关论文
共 103 条
[1]   β-Amyloid-induced glial expression of both pro- and anti-inflammatory cytokines in cerebral cortex of aged transgenic Tg2576 mice with Alzheimer plaque pathology [J].
Apelt, J ;
Schliebs, R .
BRAIN RESEARCH, 2001, 894 (01) :21-30
[2]   Conditional deletion of the TGF-β type II receptor in Col2a expressing cells results in defects in the axial skeleton without alterations in chondrocyte differentiation or embryonic development of long bones [J].
Baffi, MO ;
Slattery, E ;
Sohn, P ;
Moses, HL ;
Chytil, A ;
Serra, R .
DEVELOPMENTAL BIOLOGY, 2004, 276 (01) :124-142
[3]  
Berse B, 1999, CLIN EXP IMMUNOL, V115, P176
[4]   TGF-β signaling in fibroblasts modulates the oncogenic potential of adjacent epithelia [J].
Bhowmick, NA ;
Chytil, A ;
Plieth, D ;
Gorska, AE ;
Dumont, N ;
Shappell, S ;
Washington, MK ;
Neilson, EG ;
Moses, HL .
SCIENCE, 2004, 303 (5659) :848-851
[5]   Transforming growth factor β receptor type II inactivation promotes the establishment and progression of colon cancer [J].
Biswas, S ;
Chytil, A ;
Washington, K ;
Romero-Gallo, J ;
Gorska, AE ;
Wirth, PS ;
Gautam, S ;
Moses, HL ;
Grady, WM .
CANCER RESEARCH, 2004, 64 (14) :4687-4692
[6]   TRANSFORMING GROWTH-FACTOR-BETA BOUND TO SOLUBLE DERIVATIVES OF THE BETA-AMYLOID PRECURSOR PROTEIN OF ALZHEIMERS-DISEASE [J].
BODMER, S ;
PODLISNY, MB ;
SELKOE, DJ ;
HEID, I ;
FONTANA, A .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1990, 171 (02) :890-897
[7]  
Burt David W., 1994, Progress in Growth Factor Research, V5, P99
[8]   TGF-β receptor controls B cell responsiveness and induction of IgA in vivo [J].
Cazac, BB ;
Roes, J .
IMMUNITY, 2000, 13 (04) :443-451
[9]   TRANSFORMING GROWTH-FACTOR-BETA PROTECTS HUMAN NEURONS AGAINST BETA-AMYLOID-INDUCED INJURY [J].
CHAO, CC ;
HU, SX ;
KRAVITZ, FH ;
TSANG, M ;
ANDERSON, WR ;
PETERSON, PK .
MOLECULAR AND CHEMICAL NEUROPATHOLOGY, 1994, 23 (2-3) :159-178
[10]   SERUM CYTOKINE LEVELS IN PATIENTS WITH ALZHEIMERS-DISEASE [J].
CHAO, CC ;
ALA, TA ;
HU, SX ;
CROSSLEY, KB ;
SHERMAN, RE ;
PETERSON, PK ;
FREY, WH .
CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY, 1994, 1 (04) :433-436