Concomitance of IgM and IgG anti-dsDNA Antibodies Does Not Appear to Associate to Active Lupus Nephritis

Abstract

Previous reports proposed that the IgM anti-dsDNA antibody is protective for lupus nephritis. In this cross-sectional study, we aimed to compare clinical features of systemic lupus erythematosus (SLE) patients positive for IgG anti-dsDNA alone with those presenting both IgG and IgM anti-dsDNA. Anti-dsDNA antibodies, urinary examination and complement levels were assessed in the day of appointment. IgG and IgM anti-dsDNA antibodies were detected by indirect immunofluorescence. Fifty-eight SLE patients (93.1% female, 81% European-derived, mean age 42.8±14.7 years, mean duration of disease 10.9±8 years) positive for IgG anti-dsDNA entered the study. Of those, 15 were also positive for the IgM anti-dsDNA isotype. The group with both isotypes showed significant less frequency of active nephritis (sediment changes and proteinuria) when compared to patients with IgG anti-dsDNA alone (6.7% versus 34.9%, p=0.046). These data suggest a nephroprotective role for IgM anti-dsDNA and a distinct biologic behavior for this isotype in SLE.

B cell–intrinsic TLR9 expression is protective in murine lupus

“…Our current results nicely complement these prior studies by showing that TLR9 is required in the B cell to restrain disease. Previously, using a Wiskott Aldrich syndrome protein (WASp) model of autoimmunity, Jackson et al showed that B cell-intrinsic loss of TLR9 resulted in exacerbated disease, consistent with our and murine studies suggest that IgM anti-dsDNA antibodies are protective (60)(61)(62). Hence it remains an intriguing possibility that some TLR9-driven antibodies actually have a dominant protective effect, perhaps by promoting autoantigen clearance, partly explaining the regulatory role of TLR9.…”

Knee Joint Pain Potentially Due to Bone Alterations in a Knee Osteoarthritis Patient

“…MRI analysis revealed a medial tibial cyst during the pain-free period and broad bone signal changes in the joint at the time of severe knee pain. The OA later progressed radiographically to a more severe stage, suggesting that the cause of OA and joint pain may have been bone alterations in the knee, as also seen in a hip joint we described previously [ 2 , 3 ].…”

“…Other groups have recently described that such MRI signal changes in joints frequently suggest microfractures [ 4 , 9 , 10 ]. We also have reported that bone changes could be the primary cause of hip OA and that the pathophysiology of hip OA could be microfractures [ 2 , 3 ]. Collectively, this body of evidence strongly implicates micro-fractures with knee OA pathophysiology.…”

“…In recent studies on the relationship between OA progression and bone lesions, alterations were found to occur ahead of obvious cartilage degeneration and OA. Joint pain also frequently indicates the presence of microfractures, as do signal alterations in bones in magnetic resonance imaging (MRI) of patients with hip joint pain [ 2 , 3 ]. Although we have reported that the pathophysiology of hip OA presumably includes bone alteration, the pathogenesis of bone changes in this context is still largely unknown.…”

Combined utilization of untimed single urine of MCP-1 and TWEAK as a potential indicator for proteinuria in lupus nephritis

“…[ 19 ] TWEAK induces several nephritis-related inflammatory mediators, including Chemokine (C-C motif) ligand 5, Chemokine (C-X-C motif) ligand 10, and Vascular cell adhesion molecule-1, in the inflammatory cascade, which can cause downstream inflammatory response activation and further renal damage progression. [ 20 , 21 ] Several cross-sectional and longitudinal studies have mentioned that urinary TWEAK levels elevate in active LN patients compared with that of remission ones. [ 13 , 22 ] However, the combined utility of untimed uMCP-1 and uTWEAK still needs investigation.…”