The Anti‐Alpha‐Actinin Test Completes Anti‐DNA Determination in Systemic Lupus Erythematosus

Croquefer, Sabine; Renaudineau, Yves; Jousse, Sandrine; Guéguen, Paul; Ansart, Séverine; Saraux, Alain; Youinou, Pierre

doi:10.1196/annals.1313.017

Cited by 28 publications

(21 citation statements)

References 14 publications

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“…Overall, the mean level of Ab binding to α-actinin (by OD) in the disease subgroups was quite low. Both mean levels and cutoff levels reported here are, however, in agreement with other findings on anti α-actinin Ab binding in humans [45,47,48]. Nonetheless, it may be argued that such low OD values are not meaningful, especially as the potential pathophysiological significance of the presence of α-actinin Abs remains unclear.…”

Section: Discussionsupporting

confidence: 90%

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et al. 2006

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This study investigated the overall clinical impact of anti-α-actinin antibodies in patients with pre-selected autoimmune diseases and in a random group of anti-nuclear antibody (ANA)-positive individuals. The relation of anti-α-actinin antibodies with lupus nephritis and anti-double-stranded DNA (anti-dsDNA) antibodies represented a particular focus for the study. Using a cross-sectional design, the presence of antibodies to α-actinin was studied in selected groups, classified according to the relevant American College of Rheumatology classification criteria for systemic lupus erythematosus (SLE) (n = 99), rheumatoid arthritis (RA) (n = 68), Wegener's granulomatosis (WG) (n = 85), and fibromyalgia (FM) (n = 29), and in a random group of ANA-positive individuals (n = 142). Renal disease was defined as (increased) proteinuria with haematuria or presence of cellular casts. Sera from SLE, RA, and Sjøgren's syndrome (SS) patients had significantly higher levels of anti-α-actinin antibodies than the other patient groups. Using the geometric mean (± 2 standard deviations) in FM patients as the upper cutoff, 20% of SLE patients, 12% of RA patients, 4% of SS patients, and none of the WG patients were positive for anti-α-actinin antibodies. Within the SLE cohort, anti-α-actinin antibody levels were higher in patients with renal flares (p = 0.02) and correlated independently with anti-dsDNA antibody levels by enzyme-linked immunosorbent assay (p < 0.007) but not with other disease features. In the random ANA group, 14 individuals had anti-α-actinin antibodies. Of these, 36% had SLE, while 64% suffered from other, mostly autoimmune, disorders. Antibodies binding to α-actinin were detected in 20% of SLE patients but were not specific for SLE. They correlate with anti-dsDNA antibody levels, implying in vitro crossreactivity of anti-dsDNA antibodies, which may explain the observed association with renal disease in SLE.

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Section: Discussionsupporting

confidence: 90%

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et al. 2006

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“…46 The list includes antidsDNA, antihistones, 47-52 and antibodies versus endogenous antigens, such as antiactinin. 10,13,53,54 Actually, definition of specific renal and serum levels of the above antibodies are in progress and will be reported very soon (G.M. Ghiggeri, unpublished data).…”

Section: Discussionmentioning

confidence: 99%

Glomerular Autoimmune Multicomponents of Human Lupus Nephritis In Vivo

Bruschi¹,

Sinico

Moroni

et al. 2014

Journal of the American Society of Nephrology

100

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Renal targets of autoimmunity in human lupus nephritis (LN) are unknown. We sought to identify autoantibodies and glomerular target antigens in renal biopsy samples from patients with LN and determine whether the same autoantibodies can be detected in circulation. Glomeruli were microdissected from biopsy samples of 20 patients with LN and characterized by proteomic techniques. Serum samples from large cohorts of patients with systemic lupus erythematosus (SLE) with and without LN and other glomerulonephritides were tested. Glomerular IgGs recognized 11 podocyte antigens, with reactivity varying by LN pathology. Notably, IgG2 autoantibodies against a-enolase and annexin AI were detected in 11 and 10 of the biopsy samples, respectively, and predominated over other autoantibodies. Immunohistochemistry revealed colocalization of a-enolase or annexin AI with IgG2 in glomeruli. High levels of serum anti-a-enolase (.15 mg/L) IgG2 and/or anti-annexin AI (.2.7 mg/L) IgG2 were detected in most patients with LN but not patients with other glomerulonephritides, and they identified two cohorts: patients with high anti-a-enolase/low anti-annexin AI IgG2 and patients with low anti-a-enolase/high anti-annexin AI IgG2. Serum levels of both autoantibodies decreased significantly after 12 months of therapy for LN. Anti-a-enolase IgG2 recognized specific epitopes of a-enolase and did not cross-react with dsDNA. Furthermore, nephritogenic monoclonal IgG2 (clone H147) derived from lupus-prone MRL-lpr/lpr mice recognized human a-enolase, suggesting homology between animal models and human LN. These data show a multiantibody composition in LN, where IgG2 autoantibodies against a-enolase and annexin AI predominate in the glomerulus and can be detected in serum.

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“…The collagen-like region of C1q protein is believed to play a role in lupus nephritis and autoantibodies to this protein occur in about 30-50% of lupus patients [38]. Anti-alpha-actinin-2 antibodies have been detected in patients with lupus nephritis [40]. It was interesting that these researchers detected anti-alpha-actinin-2 antibodies even before lupus nephritis was present.…”

Section: Discussionmentioning

confidence: 99%

Diagnosis and early detection of CNS-SLE in MRL/lpr mice using peptide microarrays

2014

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BackgroundAn accurate method that can diagnose and predict lupus and its neuropsychiatric manifestations is essential since currently there are no reliable methods. Autoantibodies to a varied panel of antigens in the body are characteristic of lupus. In this study we investigated whether serum autoantibody binding patterns on random-sequence peptide microarrays (immunosignaturing) can be used for diagnosing and predicting the onset of lupus and its central nervous system (CNS) manifestations. We also tested the techniques for identifying potentially pathogenic autoantibodies in CNS-Lupus. We used the well-characterized MRL/lpr lupus animal model in two studies as a first step to develop and evaluate future studies in humans.ResultsIn study one we identified possible diagnostic peptides for both lupus and altered behavior in the forced swim test. When comparing the results of study one to that of study two (carried out in a similar manner), we further identified potential peptides that may be diagnostic and predictive of both lupus and altered behavior in the forced swim test. We also characterized five potentially pathogenic brain-reactive autoantibodies, as well as suggested possible brain targets.ConclusionsThese results indicate that immunosignaturing could predict and diagnose lupus and its CNS manifestations. It can also be used to characterize pathogenic autoantibodies, which may help to better understand the underlying mechanisms of CNS-Lupus.

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The Anti‐Alpha‐Actinin Test Completes Anti‐DNA Determination in Systemic Lupus Erythematosus

Cited by 28 publications

References 14 publications

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Glomerular Autoimmune Multicomponents of Human Lupus Nephritis In Vivo

Diagnosis and early detection of CNS-SLE in MRL/lpr mice using peptide microarrays

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