Polyclonal antibody directed against human RANTES ameliorates disease in the Lewis rat adjuvant-induced arthritis model

被引:158
作者
Barnes, DA
Tse, J
Kaufhold, M
Owen, M
Hesselgesser, J
Strieter, R
Horuk, R
Perez, HD
机构
[1] Berlex Biosci, Dept Immunol, Richmond, CA 94804 USA
[2] Berlex Biosci, Dept Pharmacol, Richmond, CA 94804 USA
[3] Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109 USA
关键词
RANTES; MIP-1; alpha; KC; arthritis; chemokine;
D O I
10.1172/JCI2172
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Adjuvant-induced arthritis (AIA) is one of many animal models of rheumatoid arthritis, a disease characterized by a T-lymphocyte and macrophage cellular infiltrate, We have characterized the development of this disease model with respect to chemokine expression. Increased levels of two chemokines, RANTES, a T-lymphocyte and monocyte chemo-attractant, and KC a chemoattractant for neutrophils, were found in whole blood and in the joint, Surprisingly, levels of MIP-1 alpha, another T-lymphocyte and monocyte chemoattractant, were unchanged throughout the course of the disease in whole blood and only slightly elevated in the joint. RANTES expression plays an important role in the disease since a polyclonal antibody to RANTES greatly ameliorated symptoms in animals induced for APA and was found to be as efficacious as treatment with indomethacin, a non-steroidal anti inflammatory. Polyclonal antibodies to either MIP-1 alpha or KC were ineffective, This is the first report to show the importance of RANTES in the development of AIA.
引用
收藏
页码:2910 / 2919
页数:10
相关论文
共 41 条
[1]   EFFECTS OF NAPROXEN ON CONNECTIVE-TISSUE CHANGES IN THE ADJUVANT ARTHRITIC RAT [J].
ACKERMAN, NR ;
ROOKS, WH ;
SHOTT, L ;
GENANT, H ;
MALONEY, P ;
WEST, E .
ARTHRITIS AND RHEUMATISM, 1979, 22 (12) :1365-1374
[2]   ACTIVATION OF DUAL T-CELL SIGNALING PATHWAYS BY THE CHEMOKINE RANTES [J].
BACON, KB ;
PREMACK, BA ;
GARDNER, P ;
SCHALL, TJ .
SCIENCE, 1995, 269 (5231) :1727-1730
[3]  
BROWN KD, 1989, J IMMUNOL, V142, P679
[4]   REQUIREMENT OF MIP-1-ALPHA FOR AN INFLAMMATORY RESPONSE TO VIRAL-INFECTION [J].
COOK, DN ;
BECK, MA ;
COFFMAN, TM ;
KIRBY, SL ;
SHERIDAN, JF ;
PRAGNELL, IB ;
SMITHIES, O .
SCIENCE, 1995, 269 (5230) :1583-1585
[5]   RED-BLOOD-CELLS ARE A SINK FOR INTERLEUKIN-8, A LEUKOCYTE CHEMOTAXIN [J].
DARBONNE, WC ;
RICE, GC ;
MOHLER, MA ;
APPLE, T ;
HEBERT, CA ;
VALENTE, AJ ;
BAKER, JB .
JOURNAL OF CLINICAL INVESTIGATION, 1991, 88 (04) :1362-1369
[6]   Seeing the wood for the trees: The forgotten role of neutrophils in rheumatoid arthritis [J].
Edwards, SW ;
Hallett, MB .
IMMUNOLOGY TODAY, 1997, 18 (07) :320-324
[7]  
FINNEY DJ, 1964, STAT METHOD BIOL ASS, P25
[8]   CYTOKINES IN CHRONIC INFLAMMATORY ARTHRITIS .1. FAILURE TO DETECT T-CELL LYMPHOKINES (INTERLEUKIN-2 AND INTERLEUKIN-3) AND PRESENCE OF MACROPHAGE COLONY-STIMULATING FACTOR (CSF-1) AND A NOVEL MAST-CELL GROWTH-FACTOR IN RHEUMATOID SYNOVITIS [J].
FIRESTEIN, GS ;
XU, WD ;
TOWNSEND, K ;
BROIDE, D ;
ALVAROGRACIA, J ;
GLASEBROOK, A ;
ZVAIFLER, NJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 1988, 168 (05) :1573-1586
[9]   HOW IMPORTANT ARE T-CELLS IN CHRONIC RHEUMATOID SYNOVITIS [J].
FIRESTEIN, GS ;
ZVAIFLER, NJ .
ARTHRITIS AND RHEUMATISM, 1990, 33 (06) :768-773
[10]   INTERLEUKIN-1 ACTIVITY IN THE SYNOVIAL-FLUID OF PATIENTS WITH RHEUMATOID-ARTHRITIS [J].
FONTANA, A ;
HENGARTNER, H ;
WEBER, E ;
FEHR, K ;
GROB, PJ ;
COHEN, G .
RHEUMATOLOGY INTERNATIONAL, 1982, 2 (02) :49-53