Project description:To examine if gene expression profiles of many Behçet’s disease (BD) patients are commonly abnormal compared to those of healthy volunteers, we performed a genome-wide complementary DNA microarray analysis using an Agilent Hu44K array; RNA samples were isolated from the PBMCs of 41 individual BD patients (32 females and 9 males) and 17 normal volunteers.
Project description:Behçet’s disease (BD) is a chronic vasculitis characterized by systemic immune aberrations. However, a comprehensive understanding of the immune disturbances in BD and how they contribute to BD pathogenesis is lacking. Here, we performed single-cell and bulk RNA sequencing to profile peripheral blood mononuclear cells (PBMCs) and isolated monocytes from BD patients and healthy controls. This dataset is the bulk RNA sequencing part (next generation sequencing-based genome-wide transcriptional profiling), which contains the transcriptional profilings of freshly isolated PBMCs from19 samples (10 healthy controls and 9 BD patients).
Project description:Behçet’s disease (BD) is a multisystemic immuno-inflammatory disorder characterized by a generalized vasculitis, particularly at the orogenital mucosa and eye. It is a complex disease with unclear pathogenesis. To better understand BD´s etiology, we performed genomic expression profiling of patients and controls. Gene expression profiling was performed in peripheral blood mononuclear cells (PBMCs) of 15 patients and 14 sex- and age-matched controls using Affymetrix microarrays. The ages of the patients and controls do not match on a one-to-one basis, but they match very well on average. The average age at examination of cases and controls is 37y.
Project description:Behçet’s disease (BD) is a chronic vasculitis characterized by systemic immune aberrations. Here, we performed single-cell sequencing to profile peripheral blood mononuclear cells (PBMCs) and isolated monocytes from BD patients and healthy donors. We observed prominent expansion and transcriptional changes in monocytes in PBMCs from BD patients. Deciphering the monocyte heterogeneity revealed the accumulation of C1q-high (C1qhi) monocytes in BD. Pseudotime inference indicated that BD monocytes markedly shifted their differentiation toward inflammation-accompanied and C1qhi monocyte-ended trajectory. Further experiments showed that C1qhi monocytes enhanced phagocytosis and proinflammatory cytokine secretion, and multi-platform analyses revealed the significant clinical relevance of this subtype. Mechanistically, C1qhi monocytes were induced by activated IFN-γ signaling in BD patients, and were decreased by tofacitinib treatment. Our study illustrates BD immune landscape and the unrecognized contribution of C1qhi monocytes to BD hyperinflammation, showing their potential as therapeutic targets and clinical assessment indexes.
Project description:Behçet’s disease (BD) is a multisystemic immuno-inflammatory disorder characterized by a generalized vasculitis, particularly at the orogenital mucosa and eye. It is a complex disease with unclear pathogenesis. To better understand BD´s etiology, we performed genomic expression profiling of patients and controls.
Project description:To examine if gene expression profiles of many Behçetâs disease (BD) patients are commonly abnormal compared to those of healthy volunteers, we performed a genome-wide complementary DNA microarray analysis using an Agilent Hu44K array; RNA samples were isolated from the PBMCs of 41 individual BD patients (32 females and 9 males) and 17 normal volunteers. A total of 41 two color arrays were performed and each individual array included a target sample and a control sample.
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:Transcriptional profiling of Homo sapiens inflammatory skin diseases (whole skin biospies): Psoriasis (Pso), vs Atopic Dermatitis (AD) vs Lichen planus (Li), vs Contact Eczema (KE), vs Healthy control (KO) In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation. In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.