Background and aims Nowadays, the definitive therapy to cure SLE has not been found yet. The newest drug available, Belimumab and Rituximab, cannot cure all kind of SLE manifestation. Moreover, both of those drugs also decrease the number of B cell in the body. Transmembrane Activator and Calcium-Modulating Cyclophillin Ligand Interactor (TACI) is an immunology based target therapy that expected to give a better result in induct remission without decreasing the number of B cell.
Aims Analyse the possibility of TACI inhibition as a targeted therapy for SLE, in order to accelerate the remission period with less side effects.
Methods We look up for scienctif article comprehensively in Medline, Science Direct, PubMed, and Cochrane Database. We found 10 article based on bibliography and keywords from the database.
Results TACI expression is elevated in B cells from patients with SLE. Inhibition of TACI cause an inhibition to B cell differentiation, and also decrease the amount of plasma cell, which cause a decreasing quantity of autoantibody which circulate in the blood. Inhibition of TACI will fully protects the animals against autoantibody production, without having any impact on B cell survival. This inhibition also delays the onset of proteinuria, albuminuria, basement membrane thickening, tubulointerstitial fibrosis, and glomerulosclerotic disease. It also inhibits only the T-cell independent responses and T-cell dependent (IgA), but it will maintain T-cell dependent protective B-cell functions.
Conclusions Inhibition of TACI may give better outcome compared to current therapy. However, the study for now is only limited in mouse.
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