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Homo sapiens

ABSTRACT: Reemergence of pathogenic, autoantibody-producing B-cell clones in myasthenia gravis following B-cell depletion therapy

PROVIDER: PRJNA886711 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21863010_subreads.fastq.gz	Fastqsanger.gz
	SRR21863011_subreads.fastq.gz	Fastqsanger.gz
	SRR21863012_subreads.fastq.gz	Fastqsanger.gz
	SRR21863013_subreads.fastq.gz	Fastqsanger.gz
	SRR21863014_subreads.fastq.gz	Fastqsanger.gz

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Reemergence of pathogenic, autoantibody-producing B-cell clones in myasthenia gravis following B-cell depletion therapy.

Project description:Myasthenia gravis (MG) is an autoantibody-mediated autoimmune disorder of the neuromuscular junction. Some patients with MG have pathogenic mAbs that recognize muscle-specific tyrosine kinase (MuSK). Patients respond well to CD20-mediated B-cell depletion therapy (BCDT); most achieve complete stable remission. However, relapse often occurs. To further understand the immunomechanisms underlying relapse we sought to study autoantibody-producing B-cells over the course of BCDT. We developed a monomeric fluorescently labelled antigen to enrich for MuSK-specific B-cells, which was validated with a novel Nalm6 cell line engineered to express a human MuSK autoantibody as B-cell receptor. We found that MuSK-specific B-cells are rare within the circulation (<3 per 10 million cells). From two MuSK-specific B-cells isolated from two distinct patients, we generated human recombinant MuSK mAbs. The autoantibodies originated from plasmablasts, used the IgG4 subclass, recognized the Ig1-like domain of MuSK and showed pathogenic capacity using an in vitro AChR clustering assay. Persistent clones of the mAbs were identified through B-cell repertoire tracing. Clonal variants of 2E6 were detected at several timepoints spanning more than five years months and reemerged after BCDT-mediated remission, appearing several months prior to relapse. These results indicate that a reservoir of rare pathogenic MuSK autoantibody-expressing B cell clones survive BCDT, then reemerge prior to manifestation of clinical relapse. This study provides both a mechanistic understanding of MuSK MG relapse and a valuable candidate biomarker for relapse prediction.

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Project description:Molecular definition of human extraocular muscles (EOM). Human EOM were compared with limb (quadriceps femoris) muscle. Keywords = Eye Keywords = EOM Keywords = Muscle Keywords = DMD Keywords = Myasthenia Gravis Keywords: other

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Project description:Autoimmune myasthenia gravis (MG) is characterized by thymic abnormalities such as hyperplasia and thymoma. Thymus plays an important role in self-tolerance and is involved in initiation and progression of the disease. A large proportion of MG patient show the presence of ectopic germinal centers (GC) in thymus that are absent in normal individuals. However, the exact mechanism how this change in thymus morphology is triggered and if this is related to pathophysiology of the disease remains unknown. In this study we have compared the mRNA profile of thymus samples obtained during a clinical trial (Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone Therapy. ClinicalTrials.gov Identifier: NCT00294658). We have compared the mRNA profile of thymus samples that have distinct germinal centers with those that lack them using Affymetrix human transcriptome array 2.0 to identify the differentially expressed genes with in the two groups.

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