Early elevations of IL-2, IL-17A, IL-22 and IFN-γ after gluten in patients with coeliac disease implicates rapidly activated T cells as their probable source.
Selected biomarkers were able to classify subjects with clear CD/non-CD status, and a subset of the biomarkers (CXCL10, GBP5, IFI27, IFNG, and UBD) showed differential expression in biopsies from subjects with no or low-grade intestinal injury that received a CD diagnosis based on biopsies taken at a later time point.
The mean serum levels of IFN-γ (p = 0.04) and IL-6 (p = 0.007) were significantly different between the patients in the CD and control groups, and IL-8 was significantly higher in the CD group compared with patients in the NCGS group (p = 0.04).
IL-18 and IFN-γ have also been implicated in the onset of different types of immune-mediate inflammatory conditions such as Type 1 Diabetes (T1D), Celiac disease (CD), rheumatoid arthritis (RA), obesity and systemic lupus erythematosus (SLE).
Proinflammatory cytokine interferon-γ and microbiome-derived metabolites dictate epigenetic switch between forkhead box protein 3 isoforms in coeliac disease.
The dental pulp plays a pivotal role in the immune defence against possible entry of pathogens from teeth, and the aim of this work was to investigate quantitative transcription levels of selected genes (IL-9, IL-11, IL-15, IL-18, IL-21, IL-27, MICA, IFN-γ) coding for pro-inflammatory immune innate activities in the pulp of primary teeth from healthy children and children with coeliac disease.
We also discovered an intricate transcriptional connectivity between CD susceptibility genes and interferon-γ, a key effector in CD, despite the absence of CD-associated SNPs in the IFNG locus.
The aims of this study were to ascertain whether five SNPs in the TNFA promoter (-1031T>C,-857C>T,-376G>A,-308G>A,-238G>A), sequence variants of the TNFRSF1A gene and IFNG +874A>T polymorphism are associated with CD in a HLA independent manner.
Interleukin (IL)-15, IL-21 and interferon-γ, cytokines over-produced in active CD, inhibited the expression of TSP-1, CD36, and CD61 in normal intestinal LPMC.
T cell lines specific for tTG and composed predominantly of CD4-positive T cells were generated from responsive CD and control individuals, and were found to produce large amounts of interferon-γ, as well as interleukins 10, 17A, and 21.
In coeliac disease (CD), the upper bowel lesion is associated with a marked infiltration of the mucosa with Th1 cells secreting interferon gamma (IFNgamma) and expressing the Th1-associated transcription factor, T-bet.
Anti-IL-15 antibody and c-jun antisense both downmodulated phospho-c-jun expression and restored TGF-beta-Smad-dependent transcription in biopsies of active celiac disease. c-jun antisense decreased interferon gamma transcription.
In conclusion, our study, which provides evidence that the effect of G on iNOS gene transcription in IFN-gamma-stimulated RAW 264.7 cells can be ascribed to all three transcription factors, may contribute to lead to new insights into the molecular mechanisms governing the inflammatory process in celiac disease.
Short term T cell lines (TCLs) obtained from treated CD biopsies cultured with gliadin with or without rhIL-10 were analysed by ELISPOT for gliadin specific production of IFN-gamma.
In order to determine whether MICA is activated in response to gliadin in patients with celiac disease (CD), small intestinal mucosa biopsy samples from ten long-standing celiac patients on a gluten-free diet and from five non-celiac individuals were incubated with and without gliadin for 4 h. Total RNA was purified and MICA, IFNG and NKG2D mRNA were quantified by fluorescent real-time RT-PCR.