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Expression data from WT CD24+CD172a+ cDC2s, WT CD24–CD172+ cDC2s, and WT CD24+CD172a– cDC1s

ABSTRACT: We used gene expression microarrays to determine if WT CD24+CD17a+ cDC2 are transcriptionally similar to WT CD172a+ cDC2

ORGANISM(S): Mus musculus

PROVIDER: GSE132767 | GEO | 2019/06/23

REPOSITORIES: GEO

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Expression data from WT CD24+CD172a+ cDC2s, WT CD24–CD172+ cDC2s, and WT CD24+CD172a– cDC1s

Project description:Expression data from WT CD24+CD172a+ cDC2s, WT CD24–CD172+ cDC2s, and WT CD24+CD172a– cDC1s

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Microarray analysis of WT and Batf3-/- CD8alpha dendritic cells from C57BL/6 spleen

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CD24+ and CD24- myeloma-derived cancer stem cell lines

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Hepatitis B virus exploits C-type lectin receptors to hijack cDC1s, cDC2s and pDCs.

Project description:ObjectivesC-type lectin receptors (CLRs) are key receptors used by DCs to orchestrate responses to pathogens. During infections, the glycan-lectin interactions shape the virus-host interplay and viruses can subvert the function of CLRs to escape antiviral immunity. Recognition of virus/viral components and uptake by CLRs together with subsequent signalling cascades are crucial in initiating and shaping antiviral immunity, and decisive in the outcome of infection. Yet, the interaction of hepatitis B virus (HBV) with CLRs remains largely unknown. As HBV hijacks DC subsets and viral antigens harbour glycan motifs, we hypothesised that HBV may subvert DCs through CLR binding.MethodsWe investigated here the pattern of CLR expression on BDCA1+ cDC2s, BDCA2+ pDCs and BDCA3+ cDC1s from both blood and liver of HBV-infected patients and explored the ability of HBsAg to bind DC subsets through specific CLRs.ResultsWe highlighted for the first time that the CLR repertoire of circulating and intrahepatic cDC2s, cDC1s and pDCs was perturbed in patients with chronic HBV infection and that some CLR expression levels correlated with plasma HBsAg and HBV DNA levels. We also identified candidate CLR responsible for HBsAg binding to cDCs (CD367/DCIR/CLEC4A, CD32/FcɣRIIA) and pDCs (CD369/DECTIN1/CLEC7A, CD336/NKp44) and demonstrated that HBsAg inhibited DC functions in a CLR- and glycosylation-dependent manner.ConclusionHBV may exploit CLR pathways to hijack DC subsets and escape from immune control. Such advances bring insights into the mechanisms by which HBV subverts immunity and pave the way for developing innovative therapeutic strategies to restore an efficient immune control of the infection by manipulating the viral glycan-lectin axis.

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Performance Evaluation of the Micromedic CD24 in Vitro Diagnostic Assay

Project description:This study is aimed to evaluate the performance of the Micromedic CD24 assay in identifying colorectal adenoma using Western blot and ELISA assays. These assays are designed to detect CD24 protein in peripheral blood leukocytes (PBL). Elevated levels of CD24 may be indicative of colorectal adenoma (inclusive of optically detectable early adenoma to late adenoma, and cancer).

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