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Role of HTLV-I infection in the pathogenesis of Sjögren's syndrome and rheumatoid arthritis.

Authors
Type
Published Article
Journal
Modern rheumatology / the Japan Rheumatism Association
Publication Date
Volume
11
Issue
2
Pages
87–90
Identifiers
DOI: 10.3109/s101650170018
PMID: 24383683
Source
Medline
License
Unknown

Abstract

Abstract HTLV-I has been identified as a causative agent which initiates and/or perpetuates the process of Sjögren's syndrome (SS) and rheumatoid arthritis (RA). A high seroprevalence of HTLV-I infection has been determined in both SS and RA patients in the HTLV-I-endemic area of Nagasaki, Japan. HTLV-I proviral DNA and HTLV-I Tax/Rex mRNA are expressed in the salivary glands or synovial cells of HTLV-I-seropositive SS or RA patients, indicating that HTLV-I is present in the affected organs and modulates the process of the disease. Cellular functions are modulated by HTLV-I infection, showing that cell proliferation and cytokine production are upregulated in HTLV-I-infected cells, and this is in part mediated by the HTLV-I Tax-induced NF-κB activation of host cells. Furthermore, Tax-mediated NF-κB activation involves resistance toward apoptotic stimuli in HTLV-I infected cells. These modulatory effects of HTLV-I Tax are believed to be important in promoting autoimmune disorders such as SS and RA in HTLV-I-seropositive subjects.

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