When versatility matters: activins/inhibins as key regulators of immunity

被引:62
作者
Aleman-Muench, G. R. [1 ]
Soldevila, G. [1 ]
机构
[1] Univ Nacl Autonoma Mexico, Inst Invest Biomed, Dept Immunol, Mexico City 04510, DF, Mexico
关键词
activin; inhibin; inflammation; immune cells; immunity; tolerance; GROWTH-FACTOR-BETA; INHIBIN-DEFICIENT MICE; ERYTHROID-DIFFERENTIATION FACTOR; MOUSE PERITONEAL-MACROPHAGES; MARROW STROMAL FIBROBLASTS; T-CELL DEVELOPMENT; ACTIVIN-A RELEASE; TGF-BETA; IN-VITRO; SIGNALING PATHWAYS;
D O I
10.1038/icb.2011.32
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Activins and inhibins are members of the transforming growth factor-beta superfamily that have been considered crucial regulators of cell processes, such as differentiation, proliferation and apoptosis, in different cell types. Initial studies about the function of activin A in the immune system focused on the regulation of hematopoiesis in the bone marrow under homeostatic and inflammatory conditions. Recent data provide a more comprehensive understanding about the role of activins/inhibins in the immune system. Novel findings included in this review point out the important requirement of activin/inhibin signaling to maintain the balance between homeostatic and inflammatory signals that are required for the optimal development and function of immune cells. The purpose of this review is to highlight the versatile nature of activins/inhibins as key regulators of both the innate and adaptive immune responses. Immunology and Cell Biology (2012) 90, 137-148; doi:10.1038/icb.2011.32; published online 3 May 2011
引用
收藏
页码:137 / 148
页数:12
相关论文
共 105 条
[1]
Abe M, 2002, J LEUKOCYTE BIOL, V72, P347
[2]
Interleukin-1 β enhances and interferon-γ suppresses activin A actions by reciprocally regulating activin A and follistatin secretion from bone marrow stromal fibroblasts [J].
Abe, M ;
Shintani, Y ;
Eto, Y ;
Harada, K ;
Fujinaka, Y ;
Kosaka, M ;
Matsumoto, T .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2001, 126 (01) :64-68
[3]
Activin receptor signaling [J].
Abe, Y ;
Minegishi, T ;
Leung, PCK .
GROWTH FACTORS, 2004, 22 (02) :105-110
[4]
Mast cell-orchestrated immunity to pathogens [J].
Abraham, Soman N. ;
St John, Ashley L. .
NATURE REVIEWS IMMUNOLOGY, 2010, 10 (06) :440-452
[5]
Activin controls skin morphogenesis and wound repair predominantly via stromal cells and in a concentration-dependent manner via keratinocytes [J].
Bamberger, C ;
Schärer, A ;
Antsiferova, M ;
Tychsen, B ;
Pankow, S ;
Müller, M ;
Rülicke, T ;
Paus, R ;
Werner, S .
AMERICAN JOURNAL OF PATHOLOGY, 2005, 167 (03) :733-747
[6]
Activin B can signal through both ALK4 and ALK7 in gonadotrope cells [J].
Bernard, Daniel J. ;
Lee, Katharine B. ;
Santos, Michelle M. .
REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY, 2006, 4 (1)
[7]
Autocrine/paracrine regulation of pituitary function by activin, inhibin and follistatin [J].
Bilezikjian, LM ;
Blount, AL ;
Leal, AMO ;
Donaldson, CJ ;
Fischer, WH ;
Vale, WW .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 2004, 225 (1-2) :29-36
[8]
SELECTIVE AND INDIRECT MODULATION OF HUMAN MULTIPOTENTIAL AND ERYTHROID HEMATOPOIETIC PROGENITOR-CELL PROLIFERATION BY RECOMBINANT HUMAN ACTIVIN AND INHIBIN [J].
BROXMEYER, HE ;
LU, L ;
COOPER, S ;
SCHWALL, RH ;
MASON, AJ ;
NIKOLICS, K .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (23) :9052-9056
[9]
Properties of inhibin binding to betaglycan, InhBP/p120 and the activin type II receptors [J].
Chapman, SC ;
Bernard, DJ ;
Jelen, J ;
Woodruff, TK .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 2002, 196 (1-2) :79-93
[10]
Chen YG, 2006, EXP BIOL MED, V231, P534