Toll-like receptors and innate immune responses in systemic lupus erythematosus

来自 NCBI

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摘要：

Pattern recognition receptors are the key to innate immune system recognition of microbes. The strength of these receptors in terms of their ability to respond to molecular motifs common to pathogens may also prove to be the weakness that results in autoimmunity, because they are potentially less discrete than the cognate immune system in distinguishing self from nonself. The most important pattern recognition receptor family of receptors involved in lupus, namely the Toll-like receptors (TLRs), can recognize a broad range of microbial components, including DNA and RNA. In this review we consider the implications of multiple studies showing how these receptors play key roles in autoimmunity in patients with systemic lupus erythematosus (SLE).Autoantibodies to DNA, RNA, and associated proteins represent a central puzzle in SLE pathogenesis. They are common targets of the autoimmune response, but the stimulus for their formation and their roles in pathogenesis have been obscure. Although exposed protein targets, such as β2-glycoprotein I and red blood cell or platelet surface proteins, can be readily implicated in pathogenesis, antibodies to nucleic acids also appear to contribute to pathology. Most notably, anti-DNA antibodies are associated with disease severity in lupus nephritis, deposit in renal tissues, crossreact with renal antigens, and can induce nephritis in mice. Anti-DNA antibodies can also crossreact with the anti-N-methyl-D-aspartate receptor and may cause cognitive dysfunction or depression in lupus patients [1,2]. Other common targets of antinuclear antibodies include proteins that bind to DNA and RNA [3]: histone proteins bind and package DNA, Sm proteins bind U RNAs and direct mRNA splicing, and Ro protein binds Y RNAs and recognizes misfolded RNAs.A common theme of autoantigens in SLE is their association in intermolecularly linked complexes associated with nucleic acids. Autoantibodies target multiple regions of autoantigens and have undergone affi

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关键词：

Humans Lupus Erythematosus, Systemic Immunity, Innate Toll-Like Receptors

DOI：

10.1186/ar2321

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年份：

2007