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Fatty Acid Amide Hydrolase regulates peripheral B cell receptor revision, polyreactivity and B1 cells in lupus

ChEBI2015-09-17 更新2026-07-12 收录

自身免疫性疾病

B细胞免疫缺陷

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-73112 数据链接链接失效反馈

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Fatty Acid Amide Hydrolase regulates peripheral B cell receptor revision, polyreactivity and B1 cells in lupus

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创建时间：

2015-09-17

表观遗传调控

B细胞免疫缺陷

Absence of Tet2 at mouse cells results in loss of hydroxymethylcytosine Hydroxymethylmethylcytosine DNA immunoprecipitation sequencing (hMeDIP-seq) of mouse TET2 WT and KO GC B-cells

NIAID Data Ecosystem80

Transcriptional profiling of human in vitro primed Th1, Th2, Th9 and Treg T cells. Transcriptional profiling of human in vitro primed Th1, Th2, Th9 and Treg T cells

T细胞亚群转录组学

自身免疫性疾病

To test whether human in vitro primed Th9 cells recapitulate the core pathogenic Th2 cell phenotype, we differentiated naïve T cells into Th1 (IL-12), Th2 (IL-4), Th9 (IL-4+TGF-β), and iTreg (TGF-β).

NIAID Data Ecosystem60

Impaired B-cell function in ERCC2 deficiency

B细胞免疫缺陷

基因变异与免疫反应

Trichothiodystrophy-1 (TTD1) is an autosomal-recessive disease and caused by mutations in ERCC2, a gene coding for a subunit of the TFIIH transcription and nucleotide-excision repair (NER) factor. In

NIAID Data Ecosystem30

CRAC channel controls the differentiation of pathogenic B cells in lupus nephritis

自身免疫性疾病

细胞分化调控

Systemic lupus erythematous (SLE) is a prototype of autoimmune disease. Lupus nephritis (LN) is one of the most serious complications of SLE. The development of autoreactive B cells and the production

NIAID Data Ecosystem60

ZBTB38 is dispensable for hematopoiesis and antibody responses.. ZBTB38 is dispensable for hematopoiesis and antibody responses.

B细胞免疫缺陷

基因功能研究

We performed RNA-sequencing of ZBTB38-sufficient and -deficient germinal center B cells. Very few genes were dysregulated by the absence of ZBTB38. Overall design: RNA-seq of ZBTB38 KO and WT germinal

NIAID Data Ecosystem40

Fatty Acid Amide Hydrolase regulates peripheral B cell receptor revision, polyreactivity and B1 cells in lupus

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