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MR Vol.11 No.2 indexに戻る
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MODERN RHEUMATOLOGY
Vol.11 No.2 |
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Role of HTLV-I infection in the pathogenesis
of Sjogren's syndrome and rheumatoid arthritis
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| A. Kawakami1, K. Eguchi1 |
| (1)First Department of Internal Medicine, Nagasaki
University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852-8501,
Japan |
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| Abstract |
| Abstract HTLV-I has been identified as a causative
agent which initiates and/or perpetuates the process of Sjogren'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-3B activation of host cells. Furthermore, Tax-mediated
NF-3B 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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| Key words |
| Key words HTLV-I ・ NF-&kgr;B ・ Rheumatoid
arthritis ・ Sjogren's syndrome ・ Tax |
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