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Several lines of evidence suggest interleukin-10 gene (IL-10) is a candidate gene in susceptibility to systemic lupus erythematosus (SLE). We investigated the association of IL-10 promoter single-nucleotide polymorphisms (SNPs) (-3575T/A,-2849G/A,-2763C/A,-1082A/G,-819T/C and-592A/C) and microsatellites (IL10.R, IL10.G) with SLE in 554 Hong Kong Chinese patients and 708 ethnically matched controls. Six haplotypes (hts) were identified from the SNPs. The genotype distribution of the ht1 (T-C-A-T-A), which is associated with low IL-10 production, was different in patients and controls (P=0.009). The homozygous genotype of non-ht1 was significantly increased in patients (P=0.009, odds ratio (OR)=1.80, 95%CI: 1.15-2.82). The frequency of IL10.G4 of IL10.G was also significantly increased in patients (P=0.017, OR=2.53, 95%CI: 1.18-5.40). We found that the homozygous non-ht1 combined with short allele (CA repeat number?21) of IL10.G has a dose-dependent effect on SLE susceptibility: non-ht1/non-ht1 with homozygous short allele showed a higher OR (OR=4.11, 95%CI: 1.27-13.2, P=0.018) of association with SLE than the genotype of non-ht1/non-ht1 with heterozygous short/long allele (OR=2.98, 95%CI: 1.26-7.07, P=0.013) and homozygous long allele (OR=1.05, 95%CI: 0.62-1.78, P=0.848). The frequency of non-ht1 was significantly increased in patients with serositis (P<0.0001, OR=2.42, 95%CI: 1.55-3.80). In conclusion, the high expression promoter genotype is associated with SLE in Chinese.Genes and Immunity (2004) 5, 484-492. doi:10.1038/sj.gene.6364119 Published online 5 August 2004 [ABSTRACT FROM AUTHOR]

Severe acute respiratory syndrome (SARS) is a recently emerged infectious disease caused by a novel coronavirus, but its immunopathological mechanisms have not yet been fully elucidated. We investigated changes in plasma T helper (Th) cell cytokines, inflammatory cytokines and chemokines in 20 patients diagnosed with SARS. Cytokine profile of SARS patients showed marked elevation of Th1 cytokine interferon (IFN)- γ, inflammatory cytokines interleukin (IL)-1, IL-6 and IL-12 for at least 2 weeks after disease onset, but there was no significant elevation of inflammatory cytokine tumour necrosis factor (TNF)- α, anti-inflammatory cytokine IL-10, Th1 cytokine IL-2 and Th2 cytokine IL-4. The chemokine profile demonstrated significant elevation of neutrophil chemokine IL-8, monocyte chemoattractant protein-1 (MCP-1), and Th1 chemokine IFN- γ-inducible protein-10 (IP-10). Corticosteroid reduced significantly IL-8, MCP-1 and IP-10 concentrations from 5 to 8 days after treatment (all P < 0·001). Together, the elevation of Th1 cytokine IFN- γ, inflammatory cytokines IL-1, IL-6 and IL-12 and chemokines IL-8, MCP-1 and IP-10 confirmed the activation of Th1 cell-mediated immunity and hyperinnate inflammatory response in SARS through the accumulation of monocytes/macrophages and neutrophils. [ABSTRACT FROM AUTHOR]

Mannose-binding lectin (MBL) is an acute-phase serum protein, and its inherited deficiency has been shown to predispose to infections. The developmental profile of serum MBL in preterm infants has been demonstrated previously. To determine the profiles of serum MBL levels and mbl2 polymorphisms over age and genders in an adult population, samples from 689 southern Chinese (age range 16–57 years; 382 males and 307 females) were studied using enzyme-linked immunosorbent assay and high-throughput genotyping of mbl2. Serum MBL levels maintained within a narrow range from age groups of 16–20 years old to 31–40 years old (mean of 2050–2160 µg/l) and declined to a mean of 1466 µg/l in the last age group 41–57 years old. No significant differences were found in the distributions of mbl2 haplotypes ( YA, XA and YB) among all these age groups. Between gender groups, no significant imbalance of MBL profile in terms of serum MBL levels and distribution of mbl2 haplotypes was found. Results suggest an important role of circulating MBL in first-line host defence because MBL maintains at fairly constant levels after childhood and no gender influence on the MBL profile. [ABSTRACT FROM AUTHOR]