Abstract:
INTRODUCTION:Rheumatic fever (RF) is an autoimmune disease caused by the gram-positive bacteria Streptococcus pyogenes that follows a nontreated throat infection in susceptible children. The disease manifests as polyarthritis, carditis, chorea, erythema marginatum, and/or subcutaneous nodules. Carditis, the most serious complication, occurs in 30% to 45% of RF patients and leads to chronic rheumatic heart disease (RHD), which is characterized by progressive and permanent valvular lesions. In this review, we will focus on the genes that confer susceptibility for developing the disease, as well as the innate and adaptive immune responses against S. pyogenes during the acute rheumatic fever episode that leads to RHD autoimmune reactions. DISCUSSION:The disease is genetically determined, and some human leukocyte antigen class II alleles are involved with susceptibility. Other single nucleotide polymorphisms for TNF-alpha and mannan-binding lectin genes were reported as associated with RF/RHD. T cells play an important role in RHD heart lesions. Several autoantigens were already identified, including cardiac myosin epitopes, vimentin, and other intracellular proteins. In the heart tissue, antigen-driven oligoclonal T cell expansions were probably the effectors of the rheumatic heart lesions. These cells are CD4(+) and produced inflammatory cytokines (TNFalpha and IFNgamma). CONCLUSION:Molecular mimicry is the mechanism that mediated the cross-reactions between streptococcal antigens and human proteins. The elucidation of chemokines and their receptors involved with the recruitment of Th1, Th2, and Th17 cells, as well as the function of T regulatory cells in situ will certainly contribute to the delineation of the real picture of the heart lesion process that leads to RHD.
journal_name
J Clin Immunoljournal_title
Journal of clinical immunologyauthors
Guilherme L,Kalil Jdoi
10.1007/s10875-009-9332-6subject
Has Abstractpub_date
2010-01-01 00:00:00pages
17-23issue
1eissn
0271-9142issn
1573-2592journal_volume
30pub_type
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journal_title:Journal of clinical immunology
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journal_title:Journal of clinical immunology
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pub_type: 临床试验,杂志文章,多中心研究
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journal_title:Journal of clinical immunology
pub_type: 临床试验,杂志文章,多中心研究,随机对照试验
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journal_title:Journal of clinical immunology
pub_type: 杂志文章
doi:10.1007/BF00915252
更新日期:1986-11-01 00:00:00
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journal_title:Journal of clinical immunology
pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:1995-09-01 00:00:00
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pub_type: 杂志文章
doi:10.1007/s10875-015-0191-z
更新日期:2015-10-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章,评审
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pub_type: 杂志文章,多中心研究
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