New biological therapies in inflammatory bowel disease

被引:15
作者
van Deventer, SJH [1 ]
机构
[1] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands
关键词
Crohn's disease; ulcerative colitis; cytokines; infliximab; T lymphocytes;
D O I
10.1053/bega.2003.0360
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Several biological therapies (monoclonal antibodies, designer molecules, recombinant cytokines) have been tested for clinical efficacy in inflammatory bowel disease, and some have been found to be effective. Anti-TNF-alpha (anti-tumour necrosis factor-alpha) antibody therapy is an important treatment modality in the treatment of active and fistulating Crohn's disease and should be considered in patients who fail standard medical therapies. Treatment with TNF-alpha-neutralizing antibodies is associated with immunosuppression that may lead to opportunistic infections and reactivation of tuberculosis, and patients should undergo Mantoux testing prior to treatment. Several other monoclonal antibodies, including anti-IL12 and anti-IFN-gamma, are currently in development for Crohn's disease. Other new approaches include ex vivo generation of regulatory T lymphocytes and antibodies that target and kill (subpopulations of) memory T lymphocytes.
引用
收藏
页码:119 / 130
页数:12
相关论文
共 108 条
[1]  
ABRAHAM E, 1999, NURSING, V29, P64
[2]  
ABRAHAM E, 1999, NURSING, V29, P59
[3]   Interleukin 10 is a growth factor for a population of regulatory T cells [J].
Asseman, C ;
Powrie, F .
GUT, 1998, 42 (02) :157-158
[4]   Blockade of interleukin 6 trans signaling suppresses T-cell resistance against apoptosis in chronic intestinal inflammation:: Evidence in Crohn disease and experimental colitis in vivo [J].
Atreya, R ;
Mudter, J ;
Finotto, S ;
Müllberg, J ;
Jostock, T ;
Wirtz, S ;
Schütz, M ;
Bartsch, B ;
Holtmann, M ;
Becker, C ;
Strand, D ;
Czaja, J ;
Schlaak, JF ;
Lehr, HA ;
Autschbach, F ;
Schürmann, G ;
Nishimoto, N ;
Yoshizaki, K ;
Ito, H ;
Kishimoto, T ;
Galle, PR ;
Rose-John, S ;
Neurath, MF .
NATURE MEDICINE, 2000, 6 (05) :583-588
[5]   Non-Th2 regulatory T-cell control of Th1 autoimmunity [J].
Bach, JF .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 2001, 54 (1-2) :21-29
[6]   IDENTITY OF TUMOR NECROSIS FACTOR AND THE MACROPHAGE-SECRETED FACTOR CACHECTIN [J].
BEUTLER, B ;
GREENWALD, D ;
HULMES, JD ;
CHANG, M ;
PAN, YCE ;
MATHISON, J ;
ULEVITCH, R ;
CERAMI, A .
NATURE, 1985, 316 (6028) :552-554
[7]   PASSIVE-IMMUNIZATION AGAINST CACHECTIN TUMOR NECROSIS FACTOR PROTECTS MICE FROM LETHAL EFFECT OF ENDOTOXIN [J].
BEUTLER, B ;
MILSARK, IW ;
CERAMI, AC .
SCIENCE, 1985, 229 (4716) :869-871
[8]   CACHECTIN TUMOR-NECROSIS-FACTOR - AN ENDOGENOUS MEDIATOR OF SHOCK AND INFLAMMATION [J].
BEUTLER, B ;
CERAMI, A .
IMMUNOLOGIC RESEARCH, 1986, 5 (04) :281-293
[9]   ULCERATIVE-COLITIS SERUM RECOGNIZES THE M(R) 40K PROTEIN ON COLONIC ADENOCARCINOMA CELLS FOR ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY [J].
BIANCONE, L ;
DAS, KM ;
ROBERTS, AI ;
EBERT, EC .
DIGESTION, 1993, 54 (04) :237-242
[10]   TUMOR-NECROSIS-FACTOR ALPHA-PRODUCING CELLS IN THE INTESTINAL-MUCOSA OF CHILDREN WITH INFLAMMATORY BOWEL-DISEASE [J].
BREESE, EJ ;
MICHIE, CA ;
NICHOLLS, SW ;
MURCH, SH ;
WILLIAMS, CB ;
DOMIZIO, P ;
WALKERSMITH, JA ;
MACDONALD, TT .
GASTROENTEROLOGY, 1994, 106 (06) :1455-1466