The diagnostic benefit of antibodies against ribosomal proteins in systemic lupus erythematosus

Shi, Zhengang; Han, Yinuo; Yin, Jing; Zhang, Yuping; Jiang, Ze-xin; Zheng, Lin; Tan, Guang; Wang, Liangchun

doi:10.1186/s42358-020-00148-2

Cited by 4 publications

(4 citation statements)

References 24 publications

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“…The ribosomal pathway is closely related to SLE. [ 31 , 32 ] A previous study showed that 15% to 35% of patients with SLE harbor ribosomal P antibodies, which are highly specific and detected in most cases of cSLE. [ 33 ] These antibodies promote the production of proinflammatory cytokines, leading to central nervous system damage, and are closely related to SLE neuropsychiatric manifestations, especially psychosis.…”

Section: Discussionmentioning

confidence: 99%

Construction of molecular subgroups in childhood systemic lupus erythematosus using bioinformatics

Zhang

Chu³

et al. 2022

Medicine

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Background: Systemic lupus erythematosus (SLE) is a complex autoimmune disorder. In patients with childhood SLE (cSLE), the onset of the disease occurs before 18 years of age and accounts for a high proportion of childhood autoimmune diseases. Adult SLE and cSLE differ in terms of clinical manifestations, gene expression profiles, and treatment. Because current diagnostic methods do not meet clinical requirements, researchers currently use transcriptome analysis to investigate the characteristics of the cSLE genome. In the present study, we used bioinformatics methods to genotype cSLE and identify potential therapeutic targets. Methods: The transcriptomes of 952 patients with cSLE and 94 normal controls were obtained from the Gene Expression Omnibus using unsupervised class learning to determine the genotypes in the microarray dataset, and the clinical characteristics, differentially expressed genes, and biological characteristics of the subtypes were analyzed. Results: Patients with cSLE were accordingly classified into three subgroups. Subgroup I was associated with lupus nephritis, female patients, and a high SLE disease activity index, and the disease in this subgroup was more severe than that in other subgroups. The SLE disease activity index in subgroup II was low; this subgroup may be related to lupus vasculitis. Subgroup III mostly included male patients and was associated with neuropsychiatric manifestations of lupus. Conclusion: We divided patients with cSLE into three subgroups with different characteristics based on transcriptome data. Our findings provide molecular evidence for future diagnosis and individualized treatment of cSLE.

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Section: Discussionmentioning

confidence: 99%

Construction of molecular subgroups in childhood systemic lupus erythematosus using bioinformatics

Zhang

Chu³

et al. 2022

Medicine

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“…Anti-ribosomal P (anti-Rib-P) antibodies are specific serological markers observed in patients [ 61 ]. Anti-ribosomal-P antibodies are located at the carboxy-terminal end of the 60S subunit of ribosomes and target three phosphorylated proteins, P0, P1, and P2 [ 62 ].…”

Section: Autoantibodies Can Lead To Neuronal Damage In Npslementioning

confidence: 99%

Neuropsychiatric Systemic Lupus Erythematosus: Molecules Involved in Its Imunopathogenesis, Clinical Features, and Treatment

Justiz-Vaillant,

Gopaul,

Soodeen

et al. 2024

Molecules

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Systemic lupus erythematosus (SLE) is an idiopathic chronic autoimmune disease that can affect any organ in the body, including the neurological system. Multiple factors, such as environmental (infections), genetic (many HLA alleles including DR2 and DR3, and genes including C4), and immunological influences on self-antigens, such as nuclear antigens, lead to the formation of multiple autoantibodies that cause deleterious damage to bodily tissues and organs. The production of autoantibodies, such as anti-dsDNA, anti-SS(A), anti-SS(B), anti-Smith, and anti-neuronal DNA are characteristic features of this disease. This autoimmune disease results from a failure of the mechanisms responsible for maintaining self-tolerance in T cells, B cells, or both. Immune complexes, circulating antibodies, cytokines, and autoreactive T lymphocytes are responsible for tissue injury in this autoimmune disease. The diagnosis of SLE is a rheumatological challenge despite the availability of clinical criteria. NPSLE was previously referred to as lupus cerebritis or lupus sclerosis. However, these terms are no longer recommended because there is no definitive pathological cause for the neuropsychiatric manifestations of SLE. Currently, the treatment options are primarily based on symptomatic presentations. These include the use of antipsychotics, antidepressants, and anxiolytic medications for the treatment of psychiatric and mood disorders. Antiepileptic drugs to treat seizures, and immunosuppressants (e.g., corticosteroids, azathioprine, and mycophenolate mofetil), are directed against inflammatory responses along with non-pharmacological interventions.

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“…Anti-ribosomal P (anti-Rib-P) antibodies are specific serological markers observed in patients [41]. Anti-ribosomal-P antibodies are located at the carboxy-terminal end of the 60S subunit of ribosomes and target three phosphorylated proteins, P0, P1, and P2 [42].…”

Section: Ribosomal P Protein (Anti-ribosmal P Ab)mentioning

confidence: 99%

Neuropsychiatric Systemic Lupus Erythematosus: Antibodies Involved, Clinical Characteristics and Treatment

Gopaul,

Vaillant

2023

Preprint

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Systemic lupus erythematosus (SLE) is a chronic idiopathic autoimmune disease affecting various organs. Patients with SLE also present numerous neuropsychiatric manifestations. These neuro-psychiatric manifestations are referred to as neuropsychiatric systemic lupus erythematosus (NPSLE). Neuropsychiatric involvement in patients with SLE was first mentioned by Kaposi more than 100 years ago and is a generic term that refers to neurological and psychiatric symp-toms resulting directly from or as a complication of SLE. NPSLE affects both the CNS and PNS and can manifest as various symptoms, such as cognitive dysfunction, organic brain syndromes, delirium, seizures, headache, and psychosis. NPSLE was previously referred to as ‘lupus cerebri-tis’ or lupus sclerosis. However, these terms are no longer recommended because there is no de-finitive pathological cause for the neuropsychiatric manifestations of SLE.[2]

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The diagnostic benefit of antibodies against ribosomal proteins in systemic lupus erythematosus

Cited by 4 publications

References 24 publications

Construction of molecular subgroups in childhood systemic lupus erythematosus using bioinformatics

Construction of molecular subgroups in childhood systemic lupus erythematosus using bioinformatics

Neuropsychiatric Systemic Lupus Erythematosus: Molecules Involved in Its Imunopathogenesis, Clinical Features, and Treatment

Neuropsychiatric Systemic Lupus Erythematosus: Antibodies Involved, Clinical Characteristics and Treatment

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