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Decreased BCMA expression on peripheral B cells according to severe disease activity suggests that BCMA plays an important regulating role in B-cell hyperactivity and immune tolerance homeostasis in SLE patients.

Cryotherapy reduced the incidence of postoperative pain and the need for medication intake in patients presenting with a diagnosis of necrotic pulp and symptomatic apical periodontitis.

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B cell activating factor (BAff) and a proliferation-inducing ligand (ApRiL) play central roles in B cell development and maturation. Soluble forms of their receptors can be generated by proteolytic cleavage; however, their physiological and clinical roles are unknown. this study aimed to assess the relationships between the receptor soluble B cell maturation antigen (sBcMA) and clinical variables in systemic lupus erythematosus (SLe) patients. Serum cytokine concentrations were measured by ELISA for 129 SLE patients and 34 healthy controls (HCs), and the expression of the receptor BCMA was evaluated on B and plasma cells from 40 subjects. SLE patients showed aberrant expression of the receptor BcMA on B and plasma cells. Soluble levels of the receptor sBcMA and its ligands sApRiL and sBAFF were increased in SLE patients compared with HCs. Additionally, sBCMA (r s = 0.6177) and sAPRIL (r s = 0.4952) correlated strongly with disease activity. Active SLE patients who achieved low disease activity showed decreased sBCMA (53.30 vs 35.30 ng/mL; p < 0.05) and sBAFF (4.48 vs 2.27 ng/mL; p < 0.05) serum levels after treatment, while sAPRIL expression remained unchanged. At a cutoff value of 22.40 ng/mL, sAPRIL showed high sensitivity (96.12%) and specificity (94.12%) for discrimination between HCs and SLE patients, while sBAFF showed lower sensitivity (82.2%) but higher specificity (94.1%) at a cutoff of 1.195 ng/mL. Relatively high levels of sAPRIL and sBCMA clustered active SLE patients. the receptor sBcMA could be a potential biomarker of disease activity in SLe.Systemic lupus erythematosus (SLE) is a chronic autoimmune disease caused by perturbations in the immune system. The extreme heterogeneity of this disease is primarily explained because genetic background confers susceptibility and environmental factors act as triggers that contribute to disease initiation and progression 1 . A key point in SLE pathogenesis is an imbalance between apoptotic cell numbers and apoptotic material disposal that leads to activation of the humoural response. The serological hallmark of SLE is the production of autoantibodies, which target antigens located in the nucleus or destined for the cell surface in the cytoplasm and are secreted by cells 2 . As T and B cell abnormalities are thought to be central to the disease process 3 , the cytokines that promote B cell differentiation and loss of tolerance have emerged as essential players in the pathophysiology of SLE 1,4 . In the regulation of B cell activation, several members of the tumour necrosis factor (TNF) superfamily participate, including B cell activating factor (BAFF) and A Proliferation-Inducing Ligand (APRIL). These stimulating factors play central roles in B cell development and maturation 5 . Altered serum levels of these cytokines have been found in autoimmune diseases such as SLE 6-11 , rheumatoid arthritis 12,13