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B-cell survival factors in autoimmune rheumatic disorders.

ABSTRACT: Autoimmune rheumatic disorders have complex etiopathogenetic mechanisms in which B cells play a central role. The importance of factors stimulating B cells, notably the B-cell activating factor (BAFF) and A proliferation inducing ligand (APRIL) axis is now recognized. BAFF and APRIL are cytokines essential for B-cell proliferation and survival from the immature stages to the development of plasma cells. Their levels are increased in some subsets of patients with autoimmune disorders. Several recent biologic drugs have been developed to block this axis, namely belimumab [already licensed for systemic lupus erythematosus (SLE) treatment], tabalumab, atacicept and blisibimod. Many clinical trials to evaluate the safety and efficacy of these drugs in several autoimmune disorders are ongoing, or have been completed recently. This review updates the information on the use of biologic agents blocking BAFF/APRIL for patients with SLE, rheumatoid arthritis, Sjögren's syndrome and myositis.

SUBMITTER: Morais SA

PROVIDER: S-EPMC4530383 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature

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B-cell survival factors in autoimmune rheumatic disorders.

Morais Sandra A SA Vilas-Boas Andreia A Isenberg David A DA

Therapeutic advances in musculoskeletal disease 20150801 4

Autoimmune rheumatic disorders have complex etiopathogenetic mechanisms in which B cells play a central role. The importance of factors stimulating B cells, notably the B-cell activating factor (BAFF) and A proliferation inducing ligand (APRIL) axis is now recognized. BAFF and APRIL are cytokines essential for B-cell proliferation and survival from the immature stages to the development of plasma cells. Their levels are increased in some subsets of patients with autoimmune disorders. Several rec ...[more]

PMID: 26288664

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Project description:BackgroundSleep disorders (SDs) in autoimmune encephalitis (AE) have received little attention and are poorly understood. We investigated the clinical characteristics, risk factors, and cerebral metabolic mechanism of SD in AE.MethodsClinical, laboratory, and imaging data were retrospectively reviewed in 121 consecutively patients with definite AE. The risk factors for SD in AE were estimated by logistic regression analysis. Group comparisons based on 18F-fluorodeoxy-glucose positron emission tomography (18F-FDG-PET) data were made between patients with and without SD, to further analyze potential brain metabolic mechanism of SD in AE.ResultsA total of 52.9% patients (64/121) with SD were identified. The multivariate logistic model analysis showed that smoking [odds ratio (OR), 6.774 (95% CI, 1.238-37.082); p = 0.027], increased Hamilton Depression scale (HAMD) score [OR, 1.074 (95% CI, 1.002-1.152); p = 0.045], hyperhomocysteinemia [OR, 2.815 (95% CI, 1.057-7.496); p = 0.038], elevated neuron-specific enolase (NSE) level [OR, 1.069 (95% CI, 1.007-1.135); p = 0.03] were independently correlated with higher risk of SD in AE patients. Contrastingly, high MoCA score [OR, 0.821 (95% CI, 0.752-0.896); p < 0.001] was associated with lower risk of SD in AE subjects. Compared to controls, AE patients had less total sleep time, less sleep efficiency, longer sleep latency, more wake, higher percent of stage N1, lower percent of stage N3 and rapid eye movement, and more arousal index in non-rapid eye movement sleep (p < 0.05 for all). Voxel-based group comparison analysis showed that, compared to patients without SD, patients with SD had increased metabolism in the basal ganglia, cerebellum, brainstem, median temporal lobe, thalamus, and hypothalamus [p < 0.05, false discovery rate (FDR) corrected]; decreased metabolism in superior frontal gyrus, medial frontal gyrus, and posterior cingulate cortex (p < 0.001, uncorrected). These results were confirmed by region of interest-based analysis between PET and sleep quality.ConclusionSmoking, increased HAMD score, hyperhomocysteinemia, and elevated NSE level were correlated with higher risk of SD. High MoCA score was associated with lower risk of SD in AE subjects. Moreover, a widespread metabolic network dysfunction may be involved in the pathological mechanism of SD in AE.

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B-cell survival factors in autoimmune rheumatic disorders.

Publications

B-cell survival factors in autoimmune rheumatic disorders.

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