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B lymphocyte alterations accompany abatacept resistance in new-onset type 1 diabetes

ABSTRACT: B lymphocyte alterations accompany abatacept resistance in new-onset type 1 diabetes

PROVIDER: PRJNA511467 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8363900.fastq.gz	Fastqsanger.gz
	SRR8363910.fastq.gz	Fastqsanger.gz
	SRR8363920.fastq.gz	Fastqsanger.gz
	SRR8363930.fastq.gz	Fastqsanger.gz
	SRR8363940.fastq.gz	Fastqsanger.gz

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B lymphocyte alterations accompany abatacept resistance in new-onset type 1 diabetes

Project description:Peripheral blood samples were collected from subjects enrolled in the TrialNet study TN-09. This was a phase II study of the effects of the T cell costimulation inhibitor CTLA4-Ig (abatacept) in new-onset T1D. Total RNA was isolated from whole blood samples and then globin-reduced. RNAseq libraries were prepared from the globin-reduced RNA.

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B lymphocyte alterations accompany abatacept resistance in new-onset type 1 diabetes.

Project description:Costimulatory interactions control T cell activation at sites of activated antigen-presenting cells, including B cells. Blockade of the CD28/CD80/CD86 costimulatory axis with CTLA4Ig (abatacept) is widely used to treat certain autoimmune diseases. While transiently effective in subjects with new-onset type 1 diabetes (T1D), abatacept did not induce long-lasting immune tolerance. To elucidate mechanisms limiting immune tolerance in T1D, we performed unbiased analysis of whole blood transcriptomes and targeted measurements of cell subset levels in subjects from a clinical trial of abatacept in new-onset T1D. We showed that individual subjects displayed age-related immune phenotypes ("immunotypes") at baseline, characterized by elevated levels of B cells or neutrophils, that accompanied rapid or slow progression, respectively, in both abatacept- and placebo-treated groups. A more pronounced immunotype was exhibited by a subset of subjects showing poor response (resistance) to abatacept. This resistance immunotype was characterized by a transient increase in activated B cells (one of the cell types that binds abatacept), reprogrammed costimulatory ligand gene expression, and reduced inhibition of anti-insulin antibodies. Our findings identify immunotypes in T1D subjects that are linked to the rate of disease progression, both in placebo- and abatacept-treated subjects. Furthermore, our results suggest therapeutic approaches to restore immune tolerance in T1D.

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