Human interleukin-19 and its receptor: a potential role in the induction of Th2 responses

被引:111
作者
Gallagher, G
Eskdale, J
Jordan, W
Peat, J
Campbell, J
Boniotto, M
Lennon, GP
Dickensheets, H
Donnelly, RP
机构
[1] Univ Med & Dent New Jersey, Dept Oral Biol, Newark, NJ 07103 USA
[2] Univ Glasgow, Dept Med, Glasgow, Lanark, Scotland
[3] US FDA, Div Therapeut Prot, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA
[4] Univ Glasgow, Dept Surg, Glasgow, Lanark, Scotland
关键词
interleukin-19; Th-2; response; induction;
D O I
10.1016/j.intimp.2004.01.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Interleukin-19 (IL-19) is a newly discovered member of the IL-10 family of ligands whose function is presently undefined. We recently described its cloning and initial characterization and in so doing, noted that the induction of IL-19 by LPS in human monocytes was down-regulated by interferon-gamma (IFN-gamma) and up-regulated by IL-4. This preliminary observation led us to speculate that IL-19 may play a role in the Th1/Th2 system and we examined this hypothesis further. Our results suggested that IL-19 is able to influence the maturation of human T-cells. CD4+ T-cells resulting from SEB stimulation in the presence of IL-19 contained a higher proportion of IL-4 producing cells than those developing in the absence of IL-19. This observation was complimented by the observation that fewer IFN-gamma cells accrued in the presence of IL-19, thereby suggesting that IL-19 altered the balance of Th1/Th2 cells in favour of Th2. Furthermore, in whole PBMC cultures, IL-19 up-regulated IL-4 and down-regulated IFNgamma in a dose-dependent manner. These results are presented here in review format, in the context of an overall discussion of IL-19 and its receptor. (C) 2004 Published by Elsevier B.V.
引用
收藏
页码:615 / 626
页数:12
相关论文
共 64 条
[1]  
AGGARWAL S, 2000, J LEUKOV BIOL, V71, P1
[2]  
Anaya JM, 2002, J RHEUMATOL, V29, P1874
[3]   Rapid clinical progression to diagnosis among African-American men with systemic lupus erythematosus [J].
Arbuckle, MR ;
James, JA ;
Dennis, GJ ;
Rubertone, MV ;
McClain, MT ;
Kim, XR ;
Harley, JB .
LUPUS, 2003, 12 (02) :99-106
[4]   Interleukin-10 promoter polymorphism in psoriasis [J].
Asadullah, K ;
Eskdale, J ;
Wiese, A ;
Gallagher, G ;
Friedrich, M ;
Sterry, W .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2001, 116 (06) :975-978
[5]   Interleukin 20: Discovery, receptor identification, and role in epidermal function [J].
Blumberg, H ;
Conklin, D ;
Xu, WF ;
Grossmann, A ;
Brender, T ;
Carollo, S ;
Eagan, M ;
Foster, D ;
Haldeman, BA ;
Hammond, A ;
Haugen, H ;
Jelinek, L ;
Kelly, JD ;
Madden, K ;
Maurer, MF ;
Parrish-Novak, J ;
Prunkard, D ;
Sexson, S ;
Sprecher, C ;
Waggie, K ;
West, J ;
Whitmore, TE ;
Yao, L ;
Kuechle, MK ;
Dale, BA ;
Chandrasekher, YA .
CELL, 2001, 104 (01) :9-19
[6]   Crystal structure of interleukin-19 defines a new subfamily of helical cytokines [J].
Chang, CS ;
Magracheva, E ;
Kozlov, S ;
Fong, S ;
Tobin, G ;
Kotenko, S ;
Wlodawer, A ;
Zdanov, A .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (05) :3308-3313
[7]   Gene microarrays reveal extensive differential gene expression in both CD4+ and CD8+ type 1 and type 2 T cells [J].
Chtanova, T ;
Kemp, RA ;
Sutherland, APR ;
Ronchese, F ;
Mackay, CR .
JOURNAL OF IMMUNOLOGY, 2001, 167 (06) :3057-3063
[8]   Interleukin-12 induces expression of interferon regulatory factor-1 via signal transducer and activator of transcription-4 in human T helper type 1 cells [J].
Coccia, EM ;
Passini, N ;
Battistini, A ;
Pini, C ;
Sinigaglia, F ;
Rogge, L .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (10) :6698-6703
[9]   Octamer proteins inhibit IL-4 gene transcription in normal human CD4 T cells [J].
Cron, RQ ;
Zhou, B ;
Brunvand, MW ;
Lewis, DB .
GENES AND IMMUNITY, 2001, 2 (08) :464-468
[10]   Cutting edge: STAT activation by IL-19, IL-20 and mda-7 through IL-20 receptor complexes of two types [J].
Dumoutier, L ;
Leemans, C ;
Lejeune, D ;
Kotenko, SV ;
Renauld, JC .
JOURNAL OF IMMUNOLOGY, 2001, 167 (07) :3545-3549