Immunomodulation: the future of allergy and asthma treatment

被引:20
作者
Bloebaum, R. Matthew [1 ]
Grant, J. Andrew [1 ]
Sur, Sanjiv [1 ]
机构
[1] Univ Texas Med Branch, Dept Internal Med, Allergy & Immunol Div, Med Res Bldg 8-104,301 Univ Blvd, Galveston, TX 77555 USA
关键词
allergic disease; asthma; immunomodulation; T helper type 2 cytokines;
D O I
10.1097/01.all.0000113681.18759.5e
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Purpose of review As the prevalence of asthma and allergic disease increases around the world, it is clear that more effective therapies and disease-modifying agents are needed. Treatment for allergic disease is evolving with an increase in understanding of the etiology. Recent findings The first immunomodulatory treatment was recently approved for use in the United States when the Food and Drug Administration approved the use of a humanized monoclonal anti-IgE antibody in patients with allergic asthma. Another strategy that has proved effective in a murine model is the downregulation of the whole immune system by targeting adhesion molecules, which has been evaluated in a recent human trial. Other strategies for the treatment of allergic diseases concentrate on refocusing the immune system away from an allergic-type response. These include the use of targeted therapies towards specific cytokines, cytokine receptors or chemokine receptors, and the use of specific bacterial DNA sequences (unmethylated cytosine-guanine dinucleotides). Finally, attention is being focused on possible therapies that may tilt the immune response to a non-allergic response by interfering with signaling molecule pathways. Summary Immunomodulation will play a key role in future therapies for allergic disease. These treatment modalities may not only treat allergic disease, but also be beneficial in reducing the morbidity and mortality for which it is responsible.
引用
收藏
页码:63 / 67
页数:5
相关论文
共 38 条
[1]  
Adachi T, 1999, J IMMUNOL, V163, P939
[2]   T(H)2 AND T(H)2-LIKE CELLS IN ALLERGY AND ASTHMA - PHARMACOLOGICAL PERSPECTIVES [J].
ANDERSON, GP ;
COYLE, AJ .
TRENDS IN PHARMACOLOGICAL SCIENCES, 1994, 15 (09) :324-332
[3]   Efficacy of soluble IL-4 receptor for the treatment of adults with asthma [J].
Borish, LC ;
Nelson, HS ;
Corren, J ;
Bensch, G ;
Busse, WW ;
Whitmore, JB ;
Agosti, JM .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2001, 107 (06) :963-970
[4]   Effects of recombinant human interleukin-12 on eosinophils, airway hyper-responsiveness, and the late asthmatic response [J].
Bryan, SA ;
O'Connor, BJ ;
Matti, S ;
Leckie, MJ ;
Kanabar, V ;
Khan, J ;
Warrington, SJ ;
Renzetti, L ;
Rames, A ;
Bock, JA ;
Boyce, MJ ;
Hansel, TT ;
Holgate, ST ;
Barnes, PJ .
LANCET, 2000, 356 (9248) :2149-2153
[5]   Omalizumab, anti-IgE recombinant humanized monoclonal antibody, for the treatment of severe allergic asthma [J].
Busse, W ;
Corren, J ;
Lanier, BQ ;
McAlary, M ;
Fowler-Taylor, A ;
Della Cioppa, G ;
van As, A ;
Gupta, N .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2001, 108 (02) :184-190
[6]   Advances in immunology - Asthma [J].
Busse, WW ;
Lemanske, RF .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (05) :350-362
[7]   Monoclonal anti-interleukin-5 treatment suppresses eosinophil but not T-cell functions [J].
Büttner, C ;
Lun, A ;
Splettstoesser, T ;
Kunkel, G ;
Renz, H .
EUROPEAN RESPIRATORY JOURNAL, 2003, 21 (05) :799-803
[8]   Omalizumab, a recombinant humanized anti-IgE antibody, reduces asthma-related emergency room visits and hospitalizations in patients with allergic asthma [J].
Corren, J ;
Casale, T ;
Deniz, Y ;
Ashby, M .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2003, 111 (01) :87-90
[9]   Discovery and structure-activity relationship of N-(ureidoalkyl)-benzyl-piperidines as potent small molecule CC chemokine receptor-3 (CCR3) antagonists [J].
De Lucca, GV ;
Kim, UT ;
Johnson, C ;
Vargo, BJ ;
Welch, PK ;
Covington, M ;
Davies, P ;
Solomon, KA ;
Newton, RC ;
Trainor, GL ;
Decicco, CP ;
Ko, SK .
JOURNAL OF MEDICINAL CHEMISTRY, 2002, 45 (17) :3794-3804
[10]   The CC chemokine antagonist Met-RANTES inhibits eosinophil effector functions through the chemokine receptors CCR1 and CCR3 [J].
Elsner, J ;
Petering, H ;
Hochstetter, R ;
Kimmig, D ;
Wells, TNC ;
Kapp, A ;
Proudfoot, AEJ .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1997, 27 (11) :2892-2898