Drug Insight: abatacept for the treatment of rheumatoid arthritis

被引：0

作者：

Eric M Ruderman

Richard M Pope

机构：

[1] Division of Rheumatology at the Northwestern University Feinberg School of Medicine,

[2] Division of Rheumatology at the Northwestern University Feinberg School of Medicine,undefined

来源：

Nature Clinical Practice Rheumatology | 2006年 / 2卷

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摘要：

Targeting the co-stimulatory signals that accompany antigen-derived signals involved in the activation of T cells represents a possible therapeutic approach for patients with rheumatoid arthritis. This Review focuses on abatacept, a fusion protein that interrupts the co-stimulatory signal mediated through the CD28–CD80/CD86 pathway, and discusses its proposed mechanism of action and outlines data from clinical trials in rheumatoid arthritis.

引用

页码：654 / 660

页数：6

共 25 条

[21]

Kremer J(2004)Cutting edge: CD28 controls peripheral homeostasis of CD4 Arthritis Rheum 50 S563-undefined

[22]

Dougados M(2006)CD25 Arthritis Rheum 54 2807-undefined

[23]

Moreland L(2004) regulatory T cells Arthritis Rheum 50 1412-undefined

[24]

Weinblatt M(undefined)CTLA-4-Ig regulates tryptophan catabolism undefined undefined undefined-undefined

[25]

Genovese MC(undefined)Sustained clinical efficacy demonstrated by the selective co-stimulation modulator abatacept (CTLA4Ig) in combination with methotrexate at 2 years in rheumatoid arthritis patients with an inadequate response to methotrexate undefined undefined undefined-undefined

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