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Effector TH17 cells give rise to long-lived TRM cells that are essential for an immediate response against bacterial infection

ABSTRACT: Effector TH17 cells give rise to long-lived TRM cells that are essential for an immediate response against bacterial infection

PROVIDER: PRJNA543753 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9090332_1.fastq.gz	Fastqsanger.gz
	SRR9090332_2.fastq.gz	Fastqsanger.gz
	SRR9090333_1.fastq.gz	Fastqsanger.gz
	SRR9090333_2.fastq.gz	Fastqsanger.gz
	SRR9090334_1.fastq.gz	Fastqsanger.gz

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Effector TH17 cells give rise to long-lived TRM cells that are essential for an immediate response against bacterial infection

Project description:Effector TH17 cells give rise to long-lived TRM cells that are essential for an immediate response against bacterial infection

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Effector TH17 cells give rise to long-lived TRM cells that are essential for an immediate response against bacterial infection

Project description:Mucosal barrier surfaces serve as the critical first line of defense separating our bodies from the plethora of pathogenic microorganisms that inhabit our environment. Adaptive immunity provides life-long protection through the generation of a central and effector memory T-cell pool, memory B cells and the recently described population of tissue resident memory cells (TRM). The cellular origin of TRM CD4 cells is unknown and the contribution of this CD4 memory population to host defense still remains elusive. By using IL-17A tracking-fate-mouse models we found that a significant fraction of the CD4 TRM cells derive from IL-17A producing effector (TH17) cells following primary immunization. Maintenance of these resting exTH17 TRM cells is mediated by IL-7, produced by lymphatic endothelial cells. During a memory response, we show that neither antibodies, nor gd T cells, nor circulatory memory T cells are sufficient for the rapid host defense required to eliminate the pathogen. Using parabiosis and depletion studies, we demonstrated that CD4 exTH17 TRM cells play an important role in respiratory defense and bacterial clearance. Upon infection, exTH17 TRM cells rapidly produce IL-17A and IFN-γ to promote neutrophil infiltration and bacterial clearance. These studies delineate the origin, function and importance of airway CD4 TRM cells during bacterial infection, offering novel strategies for targeted vaccine design, which is especially imperative for those pathogens that are resistant to antibiotic treatment.

2019-05-21 | GSE131450 | GEO

Effector TH17 cells give rise to long-lived TRM cells that are essential for an immediate response against bacterial infection

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Effector TH17 Cells Give Rise to Long-Lived TRM Cells that Are Essential for an Immediate Response against Bacterial Infection.

Project description:Adaptive immunity provides life-long protection by generating central and effector memory T cells and the most recently described tissue resident memory T (TRM) cells. However, the cellular origin of CD4 TRM cells and their contribution to host defense remain elusive. Using IL-17A tracking-fate mouse models, we found that a significant fraction of lung CD4 TRM cells derive from IL-17A-producing effector (TH17) cells following immunization with heat-killed Klebsiella pneumonia (Kp). These exTH17 TRM cells are maintained in the lung by IL-7, produced by lymphatic endothelial cells. During a memory response, neither antibodies, ?? T cells, nor circulatory T cells are sufficient for the rapid host defense required to eliminate Kp. Conversely, using parabiosis and depletion studies, we demonstrated that exTH17 TRM cells play an important role in bacterial clearance. Thus, we delineate the origin and function of airway CD4 TRM cells during bacterial infection, offering novel strategies for targeted vaccine design.

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Bone marrow-derived monocytes give rise to self-renewing and fully differentiated Kupffer cells

Project description:Self-renewing tissue-resident macrophages are thought to be exclusively derived from embryonic progenitors. However, whether circulating monocytes can also give rise to such macrophages has not been formally investigated. Here we use a new model of diphtheria toxin-mediated depletion of liver-resident Kupffer cells to generate niche availability and show that circulating monocytes engrafted in the liver, gradually adopt the transcriptional profile of their depleted counterparts and become long-lived self-renewing cells. Underlining the physiological relevance of our findings, circulating monocytes also contribute to the expanding pool of macrophages in the liver shortly after birth, when macrophage niches become available during normal organ growth. Thus, like embryonic precursors, monocytes can and do give rise to self-renewing tissue-resident macrophages if the niche is available to them. Clec4F+ Kupffer cells were isolated and sorted from livers from adult WT mice or KC-DTR or KC-DTR littermate control mice +/- 50ng DT at indicated timepoints. 19 samples (arrays) in total. RNA was isolated, amplified with Nugene pico kit, converted to cDNA and then hybridised on Affymetrix GeneChip Mouse Gene 1.0 ST Arrays.

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Bone marrow-derived monocytes give rise to self-renewing and fully differentiated Kupffer cells

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