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"Interleukin (IL)-18 (interferon-g inducing factor) merupakan salah satu sitokin yang diproduksi makrofag, berperan dalam diferensiasi sel T-helper menjadi T-helper-1, dan produksi interferon g. T-helper-1 berperan dalam imunitas seluler khususnya pada infeksi virus termasuk infeksi dengue. Dilakukan studi deskriptif korelatif mengenai hubungan kadar IL-18 dengan derajat penyakit pada penderita demam dengue (DD) dan demam berdarah dengue (DBD) yang dirawat. Pada 42 subyek yang terdiri dari 20 (47,6%) penderita demam dengue dan 22 (52,3%) demam berdarah dengue (derajat I sampai IV menurut kriteria WHO tahun 1999). Didapatkan kadar IL-18 secara bermakna lebih tinggi pada DHF dibandingkan DF. Didapatkan korelasi kadar IL-18 dengan nilai hematokrit dan hitung trombosit. Studi ini menunjang kemungkinan keterlibatan IL-18 dalam patogenesis DBD pada pasien dewasa. (Med J Indones 2004; 13: 86-9)

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Interleukin (IL)-18 ( interferon-g inducing factor) is one of cytokines, produced by macrophage, take part in differentiation T-helper (Th) to Th1 and interferon g producing. T-helper1 play role in cellular immunity especially in viral infection include dengue. A descriptive correlative study has done to know the correlation between IL-18 levels and disease severity in admitted dengue fever (DF) and dengue hemorrhagic fever (DHF) patients. In 42 subjects consist of 20 (47.6%) DF and 22 (53.3%) DHF (grade I to IV WHO criteria, 1999) showed that IL-18 levels significantly higher in DHF than DF patients. There are significant correlation between IL-18 levels and hematocrit and low platelet value. This study supports the possible role of IL-18 in pathogenesis DHF in adults. (Med J Indones 2004; 13: 86-9)"

"Background: graves disease (GD) is the most common condition of thyrotoxicosis. The management of GD is initiated with the administration of antithyroid drugs; however, it requires a long time to achieve remission. In reality more than 50% of patients who had remission may be at risk for relapse after the drug is stopped. This study aimed to evaluate the role of clinical factors such as smoking habit, degree of ophtalmopathy, degree of thyroid enlargement; genetic factors such as CTLA 4 gene on nucleotide 49 at codon 17 of exon 1, CTLA 4 gene of promotor -318, TSHR gene polymorphism rs2268458 of intron 1; and immunological factors such as regulatory T cells (Treg) and thyroid receptor antibody (TRAb); that affecting the relapse of patients with Graves disease in Indonesia. Methods: this was a case control study, that compared 72 subjects who had relapse and 72 subjects without relapse at 12 months after cessation of antithyroid treatment, who met the inclusion criteria. Genetic polymorphism examination was performed using PCR-RFLP. The number of regulatory T cells was counted using flow cytometry analysis and ELISA was used to measure TRAb. The logistic regression was used since the dependent variables were categorical variables. Results: the analysis of this study demonstrated that there was a correlation between relapse of disease and family factors (p=0.008), age at diagnosis (p=0.021), 2nd degree of Graves ophthalmopathy (p=0.001), enlarged thyroid gland, which exceeded the lateral edge of the sternocleidomastoid muscles (p=0.040), duration of remission period (p=0.029), GG genotype of CTLA 4 gene on the nucleotide 49 at codon 17 of exon 1 (p=0.016), CC genotype of TSHR gene on the rs2268458 of intron 1 (p=0.003), the number of regulatory T cells (p=0.001) and TRAb levels (p=0.002). Conclusion: genetic polymorphisms of CTLA 4 gene on the nucleotide 49 at codon 17 of exon 1, TSHR gene SNP rs2268458 of intron 1, number of regulatory T cells and TRAb levels play a role as risk factors for relapse in patients with Graves disease."

"Background: HIV infection in HCV-infected patients accelerates disease progression and reduces the success rate of Peg-IFN/RBV treatment. HCV mutation in NS5A-ISDR/PKR-BD region improved the outcome in HCV monoinfection treated with Peg-IFN/RBV. SNP-IL28B polymorphism is predicted to have an effect on HCV quasispecies evolution. However, the role of NS5A mutation and SNP IL-28B in HIV-HCV coinfection is still unclear. The aim of the study is to determine the role of HCV NS5A-ISDR/PKR-BD mutation and SNP IL-28 polymorphism on the successfulness of Peg-IFN/RBV therapy in HCV-HIV coinfection.Methods: prospective cohort was performed in this study. Plasma sample were obtained from 30 and 8 patients with HCV-HIV coinfection and HCV monoinfection, respectively. PCR nucleotide sequencing was performed after RNA virus extraction and cDNA synthesis. Protein secondary structure and prediction of mutation function were analyzed using PredictProtein (PP) program.Results: sixteen HCV-HIV coinfected patients and none from eight HCV patients achieved sustained virological response (SVR). ≥1 non-neutral mutation was found in 24/30 HCV-HIV coinfection and more frequent in SVR group (14 patients). ≥1 non-neutral mutation were found statistically significant for overall SVR achievement (p<0.05) in all patients regardless of coinfection or monoinfection status. Of the 27 HCV-HIV coinfected patients with CC-gene, 21 subjects had non-neutral mutation. The structure which was expected as NS5A binding site structure was different from consensus (wild type) in SVR group, while the structure was similar to consensus in non-SVR group.Conclusion: having ≥1 non-neutral mutation was associated with SVR achievement in Peg-IFN/RBV therapy, regardless of monoinfection and coinfection status."