Innate immunity and rheumatoid arthritis.
Innate immunity and rheumatoid arthritis.
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DOI：
10.1016/j.rdc.2010.03.004
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发表时间：
2010-05
影响因子：
2.3
通讯作者：
Pope, Richard M.
中科院分区：
文献类型：
--
作者：
Gierut, Angelica;Perlman, Harris;Pope, Richard M.
Although environmental insults such as smoking have been implicated in the initiation of rheumatoid arthritis (RA) in patients who express the shared epitope, our understanding of the role of innate immunity in the pathogenesis of this disease is also expanding. The clinical picture of pain, stiffness, swelling, and joint destruction seen in RA is a result of chronic inflammation of the synovium, characterized by interactions of fibroblast-like synoviocytes with cells of the innate immune system, including macrophages, dendritic cells, mast cells and NK cells, as well as cells of the adaptive immune system, B and T lymphocytes (1). Also present are immune complexes, proteins of the complement system, autocrine and paracrine-acting cytokines as well as chemokines that have inflammatory, homeostatic, and even antiinflammatory properties (2). As knowledge of the complexities of RA grows, gaps in the understanding of its pathogenesis are filled, and new potential therapeutic targets are uncovered.The best known function of the innate immune system is the initial recognition of microbial pathogens. Upon encounter with non-self, primarily by macrophages and dendritic cells via membrane-bound or intracellular pattern recognition receptors (PRRs), cells of the innate system become activated leading to the production of inflammatory cytokines and chemokines. Effector cells and molecules of the innate system are recruited locally, and if unable to overcome the pathogen alone, macrophages and dendritic cells travel to local lymphoid tissues. There, processed antigens are presented by MHC molecules to naïve T-cells, thus initiating an adaptive response complete with lasting immunological memory. Upon clearance of the organism, with the help of opposing anti-inflammatory mediators, the inflammatory response is terminated (3). In RA however,“self” is either the primary target, or an innocent bystander that then becomes the focus of attack. In RA there is abundant evidence that the innate immune system is persistently activated, as evidenced by the continual expression of macrophage derived cytokines such as TNFα, IL-1 and IL-6. As our understanding of the innate immune system in RA continues to expand, enticing targets for new therapeutic interventions continue to be identified. This review will focus on cells of myelomonocytic origin, their receptors and factors that interact with them.
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影响因子：
4.4
作者：
Corr, M;Crain, B
通讯作者：
Crain, B
影响因子：
15.9
作者：
Abdollahi-Roodsaz, Shahla;Joosten, Leo A. B.;Van den Berg, Wim B.
通讯作者：
Van den Berg, Wim B.
影响因子：
3.9
作者：
Bresnihan, Barry;Pontifex, Eliza;Tak, Paul-Peter
通讯作者：
Tak, Paul-Peter
影响因子：
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作者：
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通讯作者：
SALONEN, JT
影响因子：
27.4
作者：
Biro, Eva;Nieuwland, Rienk;Hack, C. Erik
通讯作者：
Hack, C. Erik