Essential role of TNF receptor superfamily 25 (TNFRSF25) in the development of allergic lung inflammation

被引:144
作者
Fang, Lei [1 ]
Adkins, Becky [1 ]
Deyev, Vadim [1 ]
Podack, Eckhard R. [1 ]
机构
[1] Univ Miami, Leonard Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA
关键词
D O I
10.1084/jem.20072528
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We identify the tumor necrosis factor receptor superfamily 25 (TNFRSF25)/TNFSF15 pair as critical trigger for allergic lung inflammation, which is a cardinal feature of asthma. TNFRSF25 (TNFR25) signals are required to exert T helper cell 2 (Th2) effector function in Th2-polarized CD4 cells and co-stimulate interleukin (IL)-13 production by glycosphingo-lipid-activated NKT cells. In vivo, antibody blockade of TNFSF15 (TL1A), which is the ligand for TNFR25, inhibits lung inflammation and production of Th2 cytokines such as IL-13, even when administered days after airway antigen exposure. Similarly, blockade of TNFR25 by a dominant-negative (DN) transgene, DN TNFR25, confers resistance to lung inflammation in mice. Allergic lung inflammation-resistant, NKT-deficient mice become susceptible upon adoptive transfer of wild-type NKT cells, but not after transfer of DN TNFR25 transgenic NKT cells. The TNFR25/TL1A pair appears to provide an early signal for Th2 cytokine production in the lung, and therefore may be a drug target in attempts to attenuate lung inflammation in asthmatics.
引用
收藏
页码:1037 / 1048
页数:12
相关论文
共 41 条
[1]   Essential role of NKT cells producing IL-4 and IL-13 in the development of allergen-induced airway hyperreactivity [J].
Akbari, O ;
Stock, P ;
Meyer, E ;
Kronenberg, M ;
Sidobre, S ;
Nakayama, T ;
Taniguchi, M ;
Grusby, MJ ;
DeKruyff, RH ;
Umetsu, DT .
NATURE MEDICINE, 2003, 9 (05) :582-588
[2]   Cutting edge:: Itk-dependent signals required for CD4+ T cells to exert, but not gain, Th2 effector function [J].
Au-Yeung, Byron B. ;
Katzman, Shoshana D. ;
Fowell, Deborah J. .
JOURNAL OF IMMUNOLOGY, 2006, 176 (07) :3895-3899
[3]   Expression, localization, and functional activity of TL1A, a novel Th1-polarizing cytokine in inflammatory bowel disease [J].
Bamias, G ;
Martin, C ;
Marini, M ;
Hoang, S ;
Mishina, M ;
Ross, WG ;
Sachedina, MA ;
Friel, CM ;
Mize, J ;
Bickston, SJ ;
Pizarro, TT ;
Wei, P ;
Cominelli, F .
JOURNAL OF IMMUNOLOGY, 2003, 171 (09) :4868-4874
[4]   Role of TL1A and its receptor DR3 in two models of chronic murine ileitis [J].
Bamias, Giorgos ;
Mishina, Margarita ;
Nyce, Mark ;
Ross, William G. ;
Kollias, Giorgos ;
Rivera-Nieves, Jesus ;
Pizarro, Theresa T. ;
Cominelli, Fabio .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (22) :8441-8446
[5]   HUMAN EOSINOPHILS IN CULTURE UNDERGO A STRIKING AND RAPID SHRINKAGE DURING APOPTOSIS - ROLE OF K+ CHANNELS [J].
BEAUVAIS, F ;
MICHEL, L ;
DUBERTRET, L .
JOURNAL OF LEUKOCYTE BIOLOGY, 1995, 57 (06) :851-855
[6]   TRAMP, a novel apoptosis-mediating receptor with sequence homology to tumor necrosis factor receptor 1 and Fas(Apo-1/CD95) [J].
Bodmer, JL ;
Burns, K ;
Schneider, P ;
Hofmann, K ;
Steiner, V ;
Thome, M ;
Bornand, T ;
Hahne, M ;
Schroter, M ;
Becker, K ;
Wilson, A ;
French, LE ;
Browning, JL ;
MacDonald, HR ;
Tschopp, J .
IMMUNITY, 1997, 6 (01) :79-88
[7]   A NOVEL PROTEIN THAT INTERACTS WITH THE DEATH DOMAIN OF FAS/APO1 CONTAINS A SEQUENCE MOTIF RELATED TO THE DEATH DOMAIN [J].
BOLDIN, MP ;
VARFOLOMEEV, EE ;
PANCER, Z ;
METT, IL ;
CAMONIS, JH ;
WALLACH, D .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (14) :7795-7798
[8]   Suppression of collagen-induced arthritis by natural killer T cell activation with OCK a sphingosine-truncated analog of α-galactosylceramide [J].
Chiba, A ;
Oki, S ;
Miyamoto, K ;
Hashimoto, H ;
Yamamura, T ;
Miyake, S .
ARTHRITIS AND RHEUMATISM, 2004, 50 (01) :305-313
[9]   FADD, A NOVEL DEATH DOMAIN-CONTAINING PROTEIN, INTERACTS WITH THE DEATH DOMAIN OF FAS AND INITIATES APOPTOSIS [J].
CHINNAIYAN, AM ;
OROURKE, K ;
TEWARI, M ;
DIXIT, VM .
CELL, 1995, 81 (04) :505-512
[10]   Signal transduction by DR3, a death domain-containing receptor related to TNFR-1 and CD95 [J].
Chinnaiyan, AM ;
ORourke, K ;
Yu, GL ;
Lyons, RH ;
Garg, M ;
Duan, DR ;
Xing, L ;
Gentz, R ;
Ni, J ;
Dixit, VM .
SCIENCE, 1996, 274 (5289) :990-992