Correlation between cellular expression of complement regulatory proteins with depletion and repopulation of B-lymphocytes in peripheral blood of patients with rheumatoid arthritis treated with rituximab

Viecceli, Daniela; Garcia, Mariana Pires; Schneider, Laiana; Alegretti, Ana Paula; Silva, Cristiano Köhler; Ribeiro, André Lucas; Brenol, Claiton Viegas; Xavier, Ricardo Machado

doi:10.1016/j.rbre.2016.09.007

Cited by 6 publications

(5 citation statements)

References 34 publications

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“…After using rituximab for 6–9 months, the number of B cells began to gradually rise. The current methods are mainly 4 × 375 mg/m 2 , 2 × 1000 mg/m 2 and 375 mg/m 2 single dose therapy based on a B‐cells driven protocol (one infusion of 375 mg/m 2 , which was repeated if the concentration of B‐cells was>0.005 × 10 9 /L of total leukocytes) . Further research is needed in the aspect of the moment of strengthen rituximab treatment.…”

Section: Advanced Therapeutic Strategymentioning

confidence: 99%

Advanced therapeutics in focal and segmental glomerulosclerosis

et al. 2018

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Focal segmental glomerulosclerosis (FSGS) is a glomerulonephritis with podocyte injury. The renal prognosis of FSGS is relative poor. The overall remission rate of the FSGS patients with nephrotic syndrome to immunosuppressive treatments was reported as 47–66%, highlighting its therapeutic challenge—lacking in sufficient evidence‐based interventions. In first‐line treatment of nephrotic syndrome, daily oral prednisolone is a commonly used drug, whereas optimal treatment strategies, like indications and duration, remain controversial. Calcineurin inhibitor and cyclophosphamide are recommended in steroid‐dependent/steroid‐resistant patients. However, the high unmet need in effective immunosuppressive treatments calls for the development of new therapy methods. Rituximab, a monoclonal antibody targeting CD20 B‐cells, could increase the complete or partial remission rate, and decrease the relapse rate based on several previous studies on FSGS. In addition, the using of rituximab could potentially help the FSGS patients to stop the concomitant therapy include steroid and immunosuppressive agents. Other treatment options like adalimumab or abatacept also showed potential therapeutic effect, but still required larger Randomized Controlled Trial study to determine its efficiency and safety. Besides, expanding understanding of the genetic basis of FSGS is necessary to investigate new therapeutic agents. With the unsatisfied patients’ outcome under the current treatments, innovation should be encouraged on the treatment strategy based on Kidney Disease: Improving Global Outcomes guideline and international collaborations are required for the potential novel immunosuppressive or immunomodulatory therapies.

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Section: Advanced Therapeutic Strategymentioning

confidence: 99%

Advanced therapeutics in focal and segmental glomerulosclerosis

et al. 2018

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“…Normal cells are resistant to the complement-mediated lysis through complement regulatory proteins (CRPs), including CD55, CD59, CD46 and CD35 ( 324 ). A study showed that increased CD46 expression in peripheral B cells, but not CD35, seemed to be able to predict nonresponders ( 278 ). CD46 reduced complement-mediated lysis, one of the mechanisms of action of rituximab, thus decreasing the effectiveness of rituximab ( 278 ).…”

Section: Bdmards Blocking T Cells Cd20 and Il-6rmentioning

confidence: 99%

“…A study showed that increased CD46 expression in peripheral B cells, but not CD35, seemed to be able to predict nonresponders ( 278 ). CD46 reduced complement-mediated lysis, one of the mechanisms of action of rituximab, thus decreasing the effectiveness of rituximab ( 278 ). It is possible that CD46 inhibitor monotherapy or combined with rituximab could be an alternative strategy for nonresponders to rituximab.…”

Section: Bdmards Blocking T Cells Cd20 and Il-6rmentioning

confidence: 99%

Toward Overcoming Treatment Failure in Rheumatoid Arthritis

et al. 2021

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Rheumatoid arthritis (RA) is an autoimmune disorder characterized by inflammation and bone erosion. The exact mechanism of RA is still unknown, but various immune cytokines, signaling pathways and effector cells are involved. Disease-modifying antirheumatic drugs (DMARDs) are commonly used in RA treatment and classified into different categories. Nevertheless, RA treatment is based on a “trial-and-error” approach, and a substantial proportion of patients show failed therapy for each DMARD. Over the past decades, great efforts have been made to overcome treatment failure, including identification of biomarkers, exploration of the reasons for loss of efficacy, development of sequential or combinational DMARDs strategies and approval of new DMARDs. Here, we summarize these efforts, which would provide valuable insights for accurate RA clinical medication. While gratifying, researchers realize that these efforts are still far from enough to recommend specific DMARDs for individual patients. Precision medicine is an emerging medical model that proposes a highly individualized and tailored approach for disease management. In this review, we also discuss the potential of precision medicine for overcoming RA treatment failure, with the introduction of various cutting-edge technologies and big data.

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“…Peripheral blood lymphocytes were isolated from RA patients and controls as described (Viecceli et al, 2017). RNA from each sample was subjected to microarray analysis and hybridization according to the manufacturer's protocol (Arraystar, MD, USA).…”

Section: Analysis Of Circrna Microarraysmentioning

confidence: 99%