Significance of Antibodies Against the Native Ribosomal P Protein Complex and Recombinant P0, P1, and P2 Proteins in the Diagnosis of Chinese Patients with Systemic Lupus Erythematosus

Li, Jing; Shen, Ying; He, Jing; Jia, Ru; Wang, Xiu‐Jie; Chen, Xiaosan; Wang, Dahai; Han, Ling; Zhu, Lei; Chi, Xiaofeng; Saschenbrecker, Sandra; Dähnrich, Cornelia; Stöcker, W.; Schlumberger, Wolfgang; Li, Zhanguo

doi:10.1002/jcla.21543

Cited by 20 publications

(19 citation statements)

References 45 publications

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“…The very high titre of anti-ribosomal P antibodies in full-blown psychosis and the pronounced fall of these antibodies thereafter, concomitant with reaching clinical remission, strongly support the concept of anti-ribosomal P antibodies causing lupus psychosis, as found in an animal model [18,19] and in the majority of clinical studies [9][10][11][12][13][14][15][16]. As already described above, intrathecal anti-ribosomal P antibodies effect psychiatric disease manifestations in mice, consistent with their specific binding pattern.…”

Section: Discussionsupporting

confidence: 71%

“…These autoantibodies are directed against three highly conserved phosphorylated P proteins [8]. Auto-antibodies recognizing the ribosomal P protein (aRP), first characterized in 1985 [9], are highly specific for SLE [10,11] and are associated with disease activity and neuropsychiatric events in SLE [12]. High levels of anti-ribosomal P antibodies have been found in psychotic SLE patients [13][14][15] and in major depressive/psychotic SLE patients [10,16], although not all studies have seen such association [17].…”

Section: Introductionmentioning

confidence: 99%

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Antibodies to Ribosomal P in Lupus Psychosis Resolving after Rituximab plus Cyclophosphamide – A Case Report

Stein¹,

Conrad²,

Aringer

2013

J Clin Cell Immunol

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Background: Central nervous disease manifestations in systemic lupus erythematosus (SLE) are variable, but may be severe. A subset of these manifestations in the central nervous system (CNS) is caused by antibodies. One antibody in particular, against ribosomal P, is supposed to play a significant role in neuropsychiatric SLE, especially lupus psychosis. Our case supports this idea. Case: We present a case of a young female who developed severe lupus psychosis after discontinuation of her immunosuppressive treatment for systemic lupus erythematosus without prior central nervous or psychiatric manifestations. Cerebral imaging and liquor analysis was unremarkable, serum analysis showed high titers of both, anti-dsDNA and anti-ribosomal P antibodies. When disease could not be controlled with high dose methylprednisolone, a combination of cyclophosphamide and rituximab was administered. Approximately two weeks after the immunosuppressive combination therapy, mood stabilization and clinical recovery were apparent. After two months the patient was recovered completely. Serology showed a striking decrease in anti-ribosomal P antibodies at this time. Conclusion: The disease course of this young patient with severe lupus psychosis suggests that the effect of pulse methylprednisolone was on the blood-brain barrier, with only with a dose of 1 g q.d. being effective. Therewith, it supports the idea of lupus psychosis being caused by auto-antibodies entering the CNS. The very high titres of antiribosomal P antibodies in full-blown psychosis, and the pronounced fall of these antibodies thereafter, concomitant with reaching clinical remission, support the concept of anti-ribosomal P antibodies causing lupus psychosis.

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Antibodies to Ribosomal P in Lupus Psychosis Resolving after Rituximab plus Cyclophosphamide – A Case Report

Stein¹,

Conrad²,

Aringer

2013

J Clin Cell Immunol

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“…Anti–galectin 3 antibody levels were also higher in patients with skin lesions than in those without skin lesions, but the difference was not significant (Figures C and D). In terms of the specificity of the 2 antibodies among SLE, DM, and SSc, levels of anti–RPLP antibodies including anti‐RPLP0 have already been shown to be a specific and effective measurement in diagnosing SLE (). Therefore, we investigated whether anti–galectin 3 antibody levels were significantly higher in SLE patients, especially those with lupus lesions, than in patients with DM or SSc.…”

Section: Resultsmentioning

confidence: 99%

Association of Anti–Acidic Ribosomal Protein P0 and Anti–Galectin 3 Antibodies With the Development of Skin Lesions in Systemic Lupus Erythematosus

Shi

Tan

Meng

et al. 2014

Arthritis & Rheumatology

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Objective. The specific autoantibodies and antigens that mediate systemic lupus erythematosus (SLE)-related organ injuries remain largely unknown. This study was undertaken to investigate the antibodymediated immune response that leads to SLE skin lesions.Methods. The study included 85 SLE patients with lupus-specific skin lesions and 31 without skin lesions. The reactivity of serum antibody with skin antigens was determined by immunoblotting using human foreskin as the substrate. Skin antigens were identified using mass spectrometry. Serum antibody was isolated by affinity purification and was injected intracutaneously into mouse skin to determine pathogenicity. Serum antibody levels were monitored by enzyme-linked immunosorbent assay.Results. We determined that 78% of the patients with skin lesions had serum antibodies reactive with 35-kd and/or 25-kd skin antigens, which was significantly higher than the percentage of patients without skin lesions (P < 0.0001), suggesting a correlation between immune response and skin lesions. Acidic ribosomal protein P0 (RPLP0) and galectin 3 were 2 target antigens identified from 35-kd and 25-kd proteins, respectively. Purified serum anti-RPLP0 and anti-galectin 3 antibodies induced lupus-like histologic changes after intracutaneous injection. Anti-RPLP0 and anti-galectin 3 antibody levels were significantly higher in SLE patients than in healthy controls and decreased with skin recovery. Anti-galectin 3 antibody levels were not significantly higher in SLE patients than in patients with dermatomyositis or scleroderma, but strongly related to lupus cutaneous vasculitis. Additionally, levels of the 2 antibodies were positively correlated with leukopenia and C3 deficiency, and the anti-RPLP0 antibody level was also positively correlated with arthritis and SLE disease activity. Conclusion. Our findings indicate that the immune response mediated by serum anti-RPLP0 and anti-galectin 3 antibodies plays a key role in the pathogenesis of SLE skin lesions. These findings provide new insights into the mechanism of SLE-related organ disorders.Systemic lupus erythematosus (SLE) is a unique autoimmune disease characterized by extremely heterogeneous clinical manifestations and the most complex autoantibody profile (1-5). Autoantibodies not only serve as a marker of disease diagnosis, activity, and severity (6,7), but they also play a primary and pivotal role in the initiation and exacerbation of SLE disease (8,9). A cluster of anti-nuclear debris antibodies, including anti-double-stranded DNA (anti-dsDNA), anti-

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“…In the subgroup analyses of ethnicity, a significant association of anti-P antibody with arthritis was found in the AfricanAmerican group (OR 3.79, 95% CI 1.40-10.30, P ¼ 0.009), but not in the Caucasian (OR 1.0, 95% CI 0.66-1.66, P ¼ 0.99) or Asian (OR 1.41, 95% CI 0.79-2.51, P ¼ 0.25) groups. The heterogeneity was relatively low in European (I 2 ¼ 0%, P Heterogeneity ¼ 0.48) and African-American groups (I 2 ¼ 34%, P Heterogeneity ¼ 0.22), but was high Haddouk et al 45 * * * * --* * * 7 Gerli et al 23 * * * * * -* * * 8 Olesin´ska et al 46 * * -* ----* 4 Briani et al 47 * * * * --* -* 6 Guo et al 48 * * -* ----* 4 Wu et al 49 * * * * ----* 5 Ghirardello et al 17 * * * * --* * * 7 Tzioufas et al 50 * * * * --* * * 7 Massardo et al 36 * * * * ----* 5 Barkhudarova et al 51 * * * * -* * -* 7 Li et al 13 * * * * -* * * * 8 Aldar et al 52 * * * --* * * * 7 Nojima et al 53 * * * * --* --5 Yalaoui et al 54 * * -* --* -* 5 Chandran et al 55 * * * * --* -* 6 Yang et al 56 * * -* ----* 4 C1: comparability1 -adjustment for disease course; C2: comparability2 -adjustment for other factors; O1: outcome1 -assessment of outcome; O2: outcome2 -adequate follow up period for outcome of interest; O3: outcome3 -adequacy of follow up of cohorts; S1: selection1 -giving the eligible criteria, sources and methods of participants; S2: selection2 -describing the characteristics of participants; S3: selection3 -defining the exposure-explicit standard for positive result; S4: demonstrating no outcome of interest at start of study.…”

Section: Association Of Anti-p Antibody With Arthritismentioning

confidence: 96%

The association of serum anti-ribosomal P antibody with clinical and serological disorders in systemic lupus erythematosus: a systematic review and meta-analysis

Shi

et al. 2014

Lupus

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Significance of Antibodies Against the Native Ribosomal P Protein Complex and Recombinant P0, P1, and P2 Proteins in the Diagnosis of Chinese Patients with Systemic Lupus Erythematosus

Cited by 20 publications

References 45 publications

Antibodies to Ribosomal P in Lupus Psychosis Resolving after Rituximab plus Cyclophosphamide – A Case Report

Antibodies to Ribosomal P in Lupus Psychosis Resolving after Rituximab plus Cyclophosphamide – A Case Report

Association of Anti–Acidic Ribosomal Protein P0 and Anti–Galectin 3 Antibodies With the Development of Skin Lesions in Systemic Lupus Erythematosus

The association of serum anti-ribosomal P antibody with clinical and serological disorders in systemic lupus erythematosus: a systematic review and meta-analysis

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