Ontology highlight
ABSTRACT:
PROVIDER: PRJNA438160 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6830890.fastq.gz | Fastqsanger.gz | |||
| SRR6830900.fastq.gz | Fastqsanger.gz | |||
| SRR6830891.fastq.gz | Fastqsanger.gz | |||
| SRR6830901.fastq.gz | Fastqsanger.gz | |||
| SRR6830892.fastq.gz | Fastqsanger.gz |
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Project description:The development of human adaptive immunity progresses faster than previously appreciated, with the emergence of memory CD4+ T cells alongside regulatory T (Treg) cells by the second trimester of pregnancy. We previously identified a prenatal-specific subset of PLZF+ CD4+ T cells with heightened effector potential that accounted for most memory T cells in the developing intestine and accumulated in the cord blood of infants exposed to prenatal inflammatory pathologies. However, the signals that drive their tissue distribution and effector maturation are unknown. Here, we define the transcriptional and functional heterogeneity of prenatal PLZF+ CD4+ T cells and identify compartmentalization of Th-like effector function across the small intestine (SI) and mesenteric lymph nodes (MLN).
2022-09-19 | GSE213522 | GEO
Project description:The development of human adaptive immunity progresses faster than previously appreciated, with the emergence of memory CD4+ T cells alongside regulatory T (Treg) cells by the second trimester of pregnancy. We previously identified a prenatal-specific subset of PLZF+ CD4+ T cells with heightened effector potential that accounted for most memory T cells in the developing intestine and accumulated in the cord blood of infants exposed to prenatal inflammatory pathologies. However, the signals that drive their tissue distribution and effector maturation are unknown. Here, we define the transcriptional and functional heterogeneity of prenatal PLZF+ CD4+ T cells and identify compartmentalization of Th-like effector function across the small intestine (SI) and mesenteric lymph nodes (MLN).
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Project description:The postnatal microbiota-immune axis establishes lifelong homeostasis at mucosal epithelial barriers. However, whether barrier-specific physiological activities regulate this process remains ill-defined. During weaning, the oral epithelium, which is monitored by Langerhans cells (LCs), is challenged by the development of a microbial plaque and the initiation of masticatory forces capable of damaging the epithelium. We demonstrate that microbial colonization following birth facilitates the differentiation of oral LCs, setting the stage for the weaning period, where adaptive immunity develops. Despite the presence of the challenging microbial plaque, LCs mainly respond to masticatory mechanical forces, inducing adaptive immunity to maintain epithelial integrity that is also associated with bone loss. Unlike adult life, this bone loss is IL-17-independent, suggesting that the establishment and maintenance of oral mucosal homeostasis involve distinct mechanisms. Moreover, barrier-specific features play a fundamental role in this early-life process.
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Project description:Mucosal associated invariant T (MAIT) cells, already differentiated and located at mucosal sites, are critical in the body’s first wave of defenses against invading pathogens. Bcl11b KO MAIT cells fail to be maintained both in the thymus and peripheral organs. Furthermore, MAIT cells fail to fully develop in the thymus without Bcl11b, failing to upregulate RORγt, and that phenotype remains in the lungs and livers of these mice. Bcl11b deletion in MAIT cells causes dramatic shifts in the activation and TH17 programs, due to the binding of Bcl11b in many of those genes, which we have seen in the human MAIT cells. MAIT cells rely on PLZF and RORγt for their development and function, while also heavily relying on Bcl11b. These data show the key interplay of Bcl11b with PLZF and RORγt in a T cell leading to its development and necessary function to protect the body against diseases.
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