期刊
LANCET INFECTIOUS DISEASES
卷 10, 期 12, 页码 875-885出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S1473-3099(10)70196-1
关键词
-
资金
- Division of Intramural Research, National Institute of Allergy and Infectious Diseases, US National Institutes of Health
Autoantibodies to cytokines occur in many different conditions and situations and can cause a wide range of disease, including pulmonary alveolar proteinosis, disseminated non-tuberculous mycobacterial disease, pure red-cell aplasia, and chronic mucocutaneous candidiasis. Anticytokine autoantibodies may also develop against exogenously administered cytokines, sometimes diminishing their effects or inhibiting the activity of the endogenous cytokine. Unlike primary congenital immunodeficiencies, autoantibodies may develop over time, wax and wane, and may change in titre or avidity. Naturally occurring autoantibodies to interferons alpha, beta, and gamma, interleukins 1 alpha, 2, 6, and 10, tumour necrosis factor, and granulocyte-macrophage colony-stimulating factor have been reported in healthy individuals and have been identified in rheumatological diseases, graft-versus-host disease, and cancer. Therapeutic antibodies, growth factors, other biological agents, and cytokines used to treat acute, chronic, malignant, and immune diseases may elicit or overcome autoantibodies, hence influencing the primary intended therapy. The increasing number of biologically active anticytokine autoantibodies being reported suggests that currently idiopathic diseases may someday be explained by neutralising or agonising autoantibodies. Their protean roles in causing, treating, preventing, and responding to disease, as well as simply maintaining normal homoeostasis, offer fascinating insights into the biology of immunity, inflammation, and infection.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据