| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2006: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2005: ¥600,000 (Direct Cost: ¥600,000)
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| Research Abstract |
In our previous study, we demonstrated the presence of IgG antibodies to triosephosphate isomerase (anti-TPI) in sera (7 of 14 patients) and in CSF (1 of 2 patients) in patients with NP lupus. Furthermore, anti-TPI antibody index has high specificity (94.5%) in patients with NP-SLE, and we concluded that anti-TPI antibody index is a clinically useful marker for NP lupus (Watanabe et al., 2004). However, the role of anti-TPI on NP lupus pathogenesis is not clear. To determine the role of anti-TPI on NP lupus pathogenesis we 1) analyzed CSF of NP lupus patients by Western blotting with anti-TPI, 2) isolated IC from CSF of NP lupus patients and investigated whether the IC contain TPI, and 3) determined C3d index in anti-TPI-positive and negative CSF of NP lupus patients and investigated whether complement activation is associated with the existence of anti-TPI in CSF of NP lupus.
We detected anti-triosephosphate isomerase antibodies (anti-TPI) in cerebrospinal fluid (CSF) in 5 of 12 neuropsychiatric lupus patients (41.6%) by Western blotting. C3d index was significantly higher in anti-TPI-positive patient (n=5, median 0.446) than in anti-TPI-negative patient (n=7, median 0.098) (p=0.019) CSF samples. TPI was detected from immune complexes (IC) isolated from CSF in 2 of 2 anti-TPI-positive patients tested and was not detected from IC in 5 of 5 anti-TPI-negative patients tested. Our results suggest that anti-TPI form IC in CSF and contribute to the pathogenesis of neuropsychiatric lupus by activating the complement system.
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