Blocking interleukin-1β in acute and chronic autoinflammatory diseases.

Blocking interleukin-1β in acute and chronic autoinflammatory diseases.
复制标题

DOI:
10.1111/j.1365-2796.2010.02313.x
复制
发表时间:
2011-01
影响因子:
11.1
通讯作者:
Dinarello CA
Dinarello CA
中科院分区:
医学1区
文献类型:
--
作者:
Dinarello CA

文献摘要

参考文献

被引文献

相似文献

急性和慢性炎性疾病的扩展谱被认为是“自身炎性”疾病。这篇综述认为自身炎症性疾病不同于“自身免疫性”疾病。自身免疫性疾病与功能失调的T细胞相关,并使用“生物制剂”治疗,包括抗TNF α、CTLA-Ig、抗IL-12/23、抗CD 20、抗IL-17和抗IL-6受体。相比之下,自身炎性疾病是由于单核细胞半胱天冬酶-1活性和IL-1β分泌功能障碍所致;事实上,阻断IL-1β导致大多数自身炎性疾病的严重程度迅速和持续降低。痛风发作、2型糖尿病、心力衰竭和郁积型多发性骨髓瘤是看似不相关的疾病的例子,这些疾病对IL-1β中和有独特的反应。
An expanding spectrum of acute and chronic inflammatory diseases are considered “autoinflammatory” diseases. This review considers autoinflammatory diseases as being distinct from “autoimmune” diseases. Autoimmune diseases are associated with dysfunctional T-cells and treated with “biologicals” including anti-TNFα, CTLA-Ig, anti-IL-12/23, anti-CD20, anti-IL-17 and anti-IL-6 receptor. In contrast, autoinflammatory diseases are uniquely due to a dysfunctional monocyte caspase-1 activity and secretion of IL-1β; indeed, blocking IL-1β results in a rapid and sustained reduction in the severity of most autoinflammatory diseases. Flares of gout, Type-2 diabetes, heart failure and smoldering multiple myeloma are examples of seemingly unrelated diseases, which are uniquely responsive to IL-1β neutralization.
DOI: 10.1084/jem.162.6.2163
发表时间: 1985-12-01
期刊: The Journal of experimental medicine
影响因子: --
作者:
Dayer JM;Beutler B;Cerami A
通讯作者: Cerami A
DOI: 10.1038/nm1603
发表时间: 2007-07-01
期刊: NATURE MEDICINE
影响因子: 82.9
作者:
Chen, Chun-Jen;Kono, Hajime;Rock, Kenneth L.
通讯作者: Rock, Kenneth L.
DOI: 10.1001/archinte.166.8.902
发表时间: 2006-04-24
影响因子: --
作者:
Bernstein, LE;Berry, J;Grinspoon, SK
通讯作者: Grinspoon, SK
DOI: 10.1210/en.2009-0543
发表时间: 2009-12-01
期刊: ENDOCRINOLOGY
影响因子: 4.8
作者:
Boeni-Schnetzler, Marianne;Boller, Simone;Donath, Marc Y.
通讯作者: Donath, Marc Y.
DOI: 10.1126/science.3086977
发表时间: 1986-06-20
期刊: SCIENCE
影响因子: 56.9
作者:
BENDTZEN, K;MANDRUPPOULSEN, T;SVENSON, M
通讯作者: SVENSON, M