Toll-like receptor 2 (TLR2), a member of the Toll-like receptor family, plays an important role in recognition of, and subsequent immune response activation against, mycobacteria. The genetic polymorphism of TLR2 (arginine to glutamine substitution at residue 753 (Arg753Gln)) has been associated with a negative influence on TLR2 function, which may, in turn, determine the innate host response to mycobacteria. The aim of the present study was to investigate the Arg753Gln single nucleotide polymorphism of the TLR2 gene in tuberculosis (TB) patients compared to healthy controls.A retrospective case/control study was carried out. The Arg753Gln polymorphism of the TLR2 gene was studied in 151 TB patients compared to 116 ethnically and agematched healthy control subjects.The TLR2 polymorphism (adenine (A) allele) was observed in 17.9 and 7.7% of TB patients and controls, respectively. When the ratios of the three genotypes were compared between the two groups, the AA genotype was found to be more significantly associated with TB. Allele frequencies for guanine (G) and A were found to be 0.95 and 0.05 in the control group and 0.86 and 0.14 in the TB patient group, respectively. The risk of developing TB disease was increased 6.04-and 1.60-fold for carriers of the AA and GA genotypes, respectively.In conclusion, the present data suggest that the arginine to glutamine substitution at residue 753 polymorphism of the Toll-like receptor 2 gene influences the risk of developing tuberculosis.

TLRs constitute an essential family of pattern recognition molecules that, through direct recognition of conserved microbial components, initiate inflammatory responses following infection. In this role, TLR1 enables host responses to a variety of bacteria, including pathogenic species of mycobacteria. In this study, we report that I602S, a common single nucleotide polymorphism within TLR1, is associated with aberrant trafficking of the receptor to the cell surface and diminished responses of blood monocytes to bacterial agonists. When expressed in heterologous systems, the TLR1 602S variant, but not the TLR1 602I variant, exhibits the expected deficiencies in trafficking and responsiveness. Among white Europeans, the 602S allele represents the most common single nucleotide polymorphism affecting TLR function identified to date. Surprisingly, the 602S allele is associated with a decreased incidence of leprosy, suggesting that Mycobacterium leprae subverts the TLR system as a mechanism of immune evasion.

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Serum IL-17 levels and IL-17 mRNA expression have been reported to be higher in psoriatic skin than normal skin. There are very limited data in the literature about difference in the levels of this cytokine in various clinical disease subtypes. We aimed to evaluate whether there is a difference in the level of this cytokine according to clinical subtypes of psoriasis. 70 psoriasis patients (30 plaque psoriasis, 20 guttate psoriasis, and 20 pustular psoriasis) and 50 age- and sex-matched healthy volunteers were included in the study. Serum IL-17 levels were determined by ELISA. Skin biopsies obtained from lesions and non-lesional skin area of 12 patients and healthy individuals (n = 5) were analyzed by quantitative PCR (qPCR) to measure the mRNA levels of IL-17. Statistically, the serum IL-17 levels did not exhibit any difference between the patients and control groups. However, analysis of each subgroup revealed that the IL-17 levels were significantly higher in pustular psoriasis group (10.09 ± 12.6 pg/ml) than controls (4.4 ± 4.1 pg/ml) (p = 0.02). In addition, the IL-17 levels of plaque psoriasis patients with PASI score ≥10 (11.30 ± 6.0 pg/ml) were significantly higher than that of patients with PASI score <10 (3.39 ± 2.6 pg/ml) and controls (p < 0.001). The Pearson correlation analysis showed a positive correlation between the serum IL-17 levels and PASI. Lesional skin samples of psoriasis patients showed significantly higher levels of IL-17 mRNA compared with perilesional skin samples (p = 0.017). Also, in the pustular psoriasis, IL-17 mRNA levels were found to be distinctively high in comparison with other clinical subtypes and healthy controls. Our results indicate that IL-17 and Th17 cells have an important role in pustular psoriasis and severe psoriasis.

Proinflammatory cytokines (such as interleukin-1beta, tumor necrosis factor-alpha) and nitric oxide are known to have both direct and indirect modulating effects on neurons and neurotoxic neurotransmitters released during excitation or inflammation. We measured interleukin-1beta, tumor necrosis factor-alpha, and nitrite levels in the peripheral blood and cerebrospinal fluid of children with febrile seizures and compared our results with those of children with febrile illnesses without seizures. Twenty-nine children with febrile seizure and 15 controls were studied. The mean concentrations of interleukin-1beta and nitrite were significantly increased in the cerebrospinal fluid (P < .01) of the children with febrile seizure. There were no significant changes in serum interleukin-1beta, tumor necrosis factor-alpha, nitrite, and cerebrospinal fluid tumor necrosis factor-alpha levels. Our data support the hypothesis that increased production of interleukin-1beta in the central nervous system or increased diffusion of interleukin-1beta through the blood-brain barrier is involved in the pathogenesis of febrile seizures.