Project description:Behçet’s Disease (BD) is a chronic and systemic vasculitis with unknown etiology. Although BD is considered a condition linking both autoimmunity and autoinflammation, aberrant innate immunity has emerged in its significant pathogenetic role, among which neutrophils directly drive inflammation in BD. To investigate neutrophil aberrance in BD, we performed bulk RNA-sequencing on isolated peripheral neutrophils from 10 pairs of BD and sex- and age-matched healthy control (HCs).
Project description:Missense mutations in the PLCg2 gene can cause autoinflammation, antibody deficiency and immune dysregulation (APLAID). Clinical and laboratory features include recurrent blistering skin lesions, pulmonary manifestations, inflammatory eye – and bowel diseases accompanied by reduced class-switching memory B cell counts and recurrent infections. Disease onset occurs typically during childhood with varying degrees of severity. To date there is no known cure of APLAID. The potential mechanism by which autoinflammation is promoted in APLAID remains elusive. However, neutrophils and macrophages are the main drivers of autoinflammation. In order to dissect the pathogenicity of disease we analyse the transcriptome of neutrophils and macrophages extracted from newly established APLAID mutant mice.
Project description:Development of Multiple Myeloma is associated with an accumulation of myeloid derived suppressor cells (MDSCs ) - cells that are morphologically and phenotypically similar to neutrophils (PMN-MDSC) and monocytes (M-MDSC), but are distinct in their functional and biochemical characteristics as well as in their ability to suppress immune responses. In our study, we found that both neutrophils and PMN-MDSCs equally promoted MM survival and decreased MM cell sensitivity to chemotherapy. Therefore, we used a microarray to elucidate the mechanism of the protective effect of neutrophils on myeloma cells.
Project description:In humans, microbial nucleic acid recognition serves as the major stimulus to an antiviral response, implying a requirement for cellular mechanisms to limit misrepresentation of self nucleic acids as non-self and the subsequent induction of type I interferon-mediated autoinflammation. This RNA-seq study was done on individuals with upregulated type I interferon signaling autoinflammatory disease.