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Peran B Cell Activating Factor (BAFF) pada Penatalaksanaan Sindrom Nefrotik : Sebuah Paradigma Baru Kristina, Astrid; Subandiyah, Krisni
Jurnal Klinik dan Riset Kesehatan Vol 3 No 1 (2023): Edisi Oktober
Publisher : RSUD Dr. Saiful Anwar Province of East Java

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.11594/jk-risk.03.1.5

Abstract

Sindrom Nefrotik (SN) adalah penyakit glomerular yang ditandai dengan proteinuria berat (≥3g/24 jam), hipoalbuminemia (≤25g/L), edema anasarka dan hiperlipidemia yang sering ditemukan. Sindrom ini dapat menyerang baik anak-anak maupun dewasa pada semua umur dan dapat disebabkan oleh penyebab idiopatik atau primer, atau penyebab sekunder akibat penyakit infeksi, penyakit sistemik, keganasan, diabetes, dan akibat obat-obatan. Terapi spesifik pada SN ditentukan oleh histopatologi dan penyebab yang mendasari. Sel B atau limfosit B adalah bagian dari kunci dalam respons kekebalan tubuh yang disebut kekebalan humoral pada mamalia. Produksi sel B pada manusia berlangsung seumur hidup, dimulai di hati janin dalam kandungan kemudian di sumsum tulang setelah lahir. Sel B berkembang dari sel induk hematopoietik. Tahapan perkembangan sel B meliputi semua tahap diferensiasi awal, pematangan, interaksi antigen, dan pada akhirnya sintesis antibodi. Selama ini, SN dianggap sebagai penyakit yang dimediasi sel T. Pandangan baru mengarah pada peran potensial sel B dalam patogenesis SN. Salah satu mekanisme yang terjadi adalah sel B menghasilkan antibodi yang mengikat antigen pada permukaan podosit yang merupakan sel khusus di glomerulus dan memainkan peran kunci dalam proses filtrasi. Baik pada Sindrom Nefrotik Sensitif Steroid (SNSS) maupun Sindrom Nefrotik Resisten Steroid (SNRS), mekanisme penyebab keduanya masih belum jelas namun diduga memiliki hubungan erat dengan gangguan sistem imunitas, terutama sel B. Dari banyaknya subpulasi sel B yang berperan, B-cell activating factor (BAFF), yang termasuk dalam golongan tumor necrosis factor (TNF), merupakan sitokin esensial yang memiliki peranan penting pada maturasi, aktivasi, dan survival limfosit B.
Vitamin D3 induces stem cell activation via Lgr5-Bmi1 expression and improving mouse colitis histology index Wibowo, Satrio; Pramadhani, Almira; Subandiyah, Krisni; Handono, Kusworini; Poeranto, Sri
Narra J Vol. 3 No. 3 (2023): December 2023
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v3i3.430

Abstract

Conventional therapy for inflammatory bowel disease using long-term anti-inflammatory drugs does not seem to provide optimal results. Adjuvant therapy using vitamin D3 is believed to have an essential role in repairing the colonic mucosa through the activation of colonic stem cells. The aim of this study was to demonstrate the effect of vitamin D3 in mucosal repair through stem cell activation, marked by leucin-rich repeat-containing G protein-coupled receptor 5 (Lgr5) and B lymphoma Mo-MLV insertion region 1 (Bmi1) expression and decrease the mouse colitis histology index (MCHI) score. In this study, 50 Mus musculus strain BALB/c were divided into five groups: negative control group, colitis group, and colitis groups with vitamin D3 administration of 0.2 mcg, 0.4 mcg, and 0.6 mcg per 25 g body weight for seven days. Dextran sulfate sodium (DSS) 5% was used to induce colitis. Lgr5-Bmi1 expression was measured using immunodoublestain fluorescent labeling method. Our data suggested that administration of vitamin D3 significantly increased expression of Lgr5-Bmi1 in the colonic mucosa. The colitis group treated with the highest dose of vitamin D3 (0.6 mcg/25 gram) showed the lowest MCHI score (3.60±0.64) while the lowest dose of vitamin D3 had the highest MCHI score (12.60±1.47). In conclusion, stimulating stem cells, vitamin D3 administration stimulates mucosal regeneration, as demonstrated by upregulated expression of Lgr5-Bmi-1.
Peran B Cell Activating Factor (BAFF) pada Penatalaksanaan Sindrom Nefrotik : Sebuah Paradigma Baru Kristina, Astrid; Subandiyah, Krisni
Jurnal Klinik dan Riset Kesehatan Vol 3 No 1 (2023): Edisi Oktober
Publisher : RSUD Dr. Saiful Anwar Province of East Java

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.11594/jk-risk.03.1.5

Abstract

Nephrotic syndrome is a glomerular disease characterized by severe proteinuria (≥3g/24 hours), hypoalbuminemia (≤25g/L), and oedema, with hyperlipidemia in some cases. This syndrome can affect both children and adults of all ages and can be caused by idiopathic or primary causes, or secondary causes due to infectious diseases, systemic diseases, malignancies, diabetes, and the effect of drugs. Specific therapy in nephrotic syndrome is determined by histopathology and the underlying cause. B cells or B lymphocytes are part of a key part of mammals' immune response called humoral immunity. Production of B cells in humans is lifelong, beginning in the fetal liver intrauterine and then in the bone marrow after birth. B cells developed from hematopoietic stem cells. The developmental stages of B cells include all stages of initial differentiation, maturation, antigen interaction, and ultimately antibody synthesis. Until recently, nephrotic syndrome was considered a T-cell-mediated disease, new insights point to the potential role of B cells in the pathogenesis of nephrotic syndrome. One of the mechanisms that occurs is that B cells produce antibodies that bind to antigens on the surface of podocytes which are special cells in the glomerulus and play a key role in the filtration process. In both SSNS and SRNS, the causal mechanism for both is still unclear but is thought to have a close relationship with immune system disorders, especially B cells.