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Background: Acne vulgaris (AV) is a chronic, multifactorial, inflammatory skin disease, and it is now becoming increasingly clear that the inflammatory pathway is involved at a very early in the pathogenesis of acne. The Th17 cells, the activators of this cell line and its downstream effector cytokines, are all likely to have a critical role in inducing and maintaining the disease. Aim: To analyse the role of interleukins (ILs) 6, 8, 17 and 22 in the pathogenesis of acne. Materials and Methods: Sixty patients of AV and thirty age- and sex-matched controls were included in our study. Serum levels of interleukins 6, 8, 17 and 22 were determined using an enzyme-linked immunosorbent assay (ELISA), and thereafter, levels were correlated with the severity of acne. Result: Serum levels of IL-6, IL-8, IL-17 and IL-22 were 0.15 ± 0.0174 pg/ml, 0.38 ± 0.080 pg/ml, 0.19 ± 0.0075 pg/ml and 0.23 ± 0.0152 pg/ml in cases, respectively, and 0.13 ± 0.0095 pg/ml, 0.14 ± 0.034 pg/ml, 0.13 ± 0.0033 pg/ml and 0.21 ± 0.0099 pg/ml in controls, respectively. The difference in levels between cases and controls was significant for IL-8 and IL-17, while for IL-6 and IL-22 the difference was insignificant. There was a highly significant positive correlation between IL-8 and IL-17 levels. IL-6 and IL-8 showed a significant positive correlation with the severity of disease. Conclusion: IL-8 and IL-17 play a critical effector role in the pathogenesis of AV. IL-6-stimulated Th17 cells are likely the major producers of IL-8 in acne lesions. [ABSTRACT FROM AUTHOR]

Multiple studies have identified the presence of peripheral immune aberrations in subjects with Autism Spectrum Disorder (ASD). However, comprehensive assessment of these peripheral immune aberrations, in the cellular and systemic compartments, in a single group of subjects with ASD is lacking. We assessed proportions of various subsets of immune cells in peripheral blood (T helper cells, T regulatory cells, B cells, monocytes, Natural Killer cells, dendritic cells) by multi-parametric flow cytometry in 50 children with ASD and compared it with thirty healthy controls matched for age, gender, socio-economic status and body mass index. There were no significant differences noted in the proportion of T regulatory cells, B cells, monocytes and Natural Killer cells, between ASD subjects and controls. On the contrary, the proportion of activated Th17 and myeloid dendritic cells were significantly higher in children with ASD. Based on these findings, group comparison of serum levels of Th17 cytokines (interleukin-6, interleukin-17A) was performed. Elevated serum levels of interleukin-6 and interleukin-17A in children with ASD corroborated our immunophenotyping findings. We did not find any significant differences among the pro-inflammatory (interleukin-1β), Th1 (interferon-γ) and Th2 (interleukin-4) cytokines. This is the first evidence with concurrent findings from immunophenotyping and cytokine data demonstrating activation of the Th17 pathway in subjects with ASD. This finding assumes significance in the light of recent maternal immune activation mouse model study that has highlighted the role of Th17 pathway in the pathophysiology of ASD. Future longitudinal studies are needed to clarify the role of this dysregulated immune pathway in the development of ASD. [ABSTRACT FROM AUTHOR]

Background & Objectives: Visceral leishmaniasis or kala-azar is a fatal protozoan disease caused by an obligate intracellular parasite, Leishmania donovani. Susceptibility, establishment of infection and severity of this disease depend upon many factors, but it is the host immune system that plays decisive role in disease progression. Keeping this view into consideration, we investigated the probable relationship between polymorphisms rs2275913 and rs8193036 in IL-17 gene, and its association as a risk factor for kala-azar in an endemic population of Assam, India., Methods: A total of 209 subjects, 76 kala-azar cases (male: 46, female: 30, mean age ± SD: 34.60 ± 12.61) and 133 controls (male: 66, female: 67, mean age ± SD: 33.35 ± 14.48) were included in this study. We analysed the polymorphisms, rs2275913 and rs8193036 by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. The data were analysed using logistic regression analysis and SPSS software., Results: The results revealed that the mutant rs8193036 TT genotype conferred 4.7-fold higher risk for kala-azar (p = 0.00991, OR = 4.72, 95% CI = 1.330-16.911). A significant difference was found between the allele frequencies of rs8193036 (p = 0.029, OR = 1.64, 95% CI = 1.04-2.57) when comparisons were done using the genetic models of association. When stratification analysis was done on the basis of active and past cases we found that during active infection rs2275913 A allele was significantly associated with increased risk of kala-azar (p = 0.016, OR = 3.95, 95% CI = 1.21-12.87)., Interpretation & Conclusion: The findings revealed that IL-17 genetic variant, rs8193036 is an independent risk factor for kala-azar infection and may contribute in pathogenesis of the disease. Further, rs2275913 polymorphism of IL-17 gene is associated with kala-azar during active infection., Competing Interests: None

Interleukin 17A (IL-17) production by peripheral blood neutrophils was examined in patients with fungal keratitis and in uninfected individuals in southern India, which has high levels of airborne Aspergillus and Fusarium conidia. Il17a gene expression and intracellular IL-17 were detected in all groups, although levels were significantly elevated in neutrophils from patients with keratitis. There were no significant differences in plasma IL-17 and IL-23 between patients with keratitis and uninfected individuals; however, combined data from all groups showed a correlation between the percentage IL-17 producing neutrophils and plasma IL-23, and between plasma IL-17 and IL-6 and IL-23., (© The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)