SummaryTo determine the cytokine balance in patients with lupus nephritis (LN) ,

Significance of antiprothrombin antibodies in patients with systemic lupus erythematosus: clinical evaluation of the antiprothrombin assay and the antiphosphatidylserine/prothrombin assay, and comparison with other antiphospholipid antibody assays Abstract Antibodies against prothrombin are detected by enzyme immunoassays (EIA) in sera of patients with antiphospholipid syndrome (APS). However, there are two methods for antiprothrombin EIA; one that uses high binding plates (aPT-A), and another that utilizes phosphatidylserine bound plates (aPS/PT). We aimed to evaluate and compare aPT-A and aPS/PT in a clinical setting. We performed EIA for anti-PT, anti-PS/PT, IgG, and IgM anticardiolipin antibodies (aCL), and IgG β2-glycoprotein I-dependent aCL (aβ2GPI/CL) with serum samples from 139 systemic lupus erythematosus (SLE) patients (16 with history of at least one thrombotic episode) and 148 controls. We observed that: (1) although titers of anti-PT and anti-PS/PT were significantly related with each other (P < 0.0001, ρ = 0.548), titer of anti-PT and anti-PS/PT differed greatly in some samples; (2) odds ratio and 95% confidence interval for each assay was 3.556 (1.221-10.355) for aPT-A, 4.591 (1.555-15.560) for aPS/ PT, for IgM aCL,) for aβ2GPI/CL. We conclude that, while all EIA performed in this study except IgM aCL are of potential value in assessing the risk of thrombosis, aPS/PT and aβ2GPI/CL seemed to be highly valuable in clinical practice, and that autoantibodies detected by anti-PT and anti-PS/PT are not completely identical.

To clarify the role of T cells in the kidneys of MRL/MpJ-lpr (MRL/lpr) mice, cytokine mRNA expression was analyzed, and tissue localization of T cells was examined by immunohistochemistry. Cells infiltrating the glomeruli, glomerular circumference, and perivascular areas in ten female MRL/lpr mice were captured by laser microdissection (LMD). Nested reverse transcription polymerase chain reaction (RT-PCR) of samples was performed with primers specific for beta-actin, T-cell receptor beta chain (TCR-Cbeta), Thy-1, B220, CD4, CD8, interleukin (IL)-2, IL-4, IL-10, IL-13, IL-17, and interferon (IFN)-gamma. Frozen sections of lesions were also stained immunohistochemically. B220, MAC-1, Thy-1, CD4, and CD8 staining was observed in glomeruli and perivascular areas, especially in glomerular circumference areas. T cells infiltrating the glomeruli, glomerular circumference areas, and perivascular areas produce INF-gamma, IL-13, and IL-17 predominately. IL-10 positivity was identified in 60% of perivascular T cells but not in a substantial number of glomerular or periglomerular T cells. The results of our study suggest that the pathogenesis of renal lesions in MRL/lpr mice is complex and not due simply to the Th1 and Th2 balance. These findings also support the concept of different molecular mechanisms for glomerulonephritis and vasculitis in these mice.

Perivascular lesions show wide distribution in patients with IgG4-RD. Serum CRP levels are not necessarily elevated in these patients. Steroid therapy is effective in IgG4-RD and results in resolution of lesions.