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Effect of fatty acid synthesis inhibition in IL-17-producing gamma delta T (γδT17) cells upon psoriatic inflammation

ABSTRACT: Effect of fatty acid synthesis inhibition in IL-17-producing gamma delta T (γδT17) cells upon psoriatic inflammation

PROVIDER: PRJNA1079810 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28074630_1.fastq.gz	Fastqsanger.gz
	SRR28074630_2.fastq.gz	Fastqsanger.gz
	SRR28074631_1.fastq.gz	Fastqsanger.gz
	SRR28074631_2.fastq.gz	Fastqsanger.gz
	SRR28074632_1.fastq.gz	Fastqsanger.gz

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Effect of fatty acid synthesis inhibition in IL-17-producing gamma delta T (γδT17) cells upon psoriatic inflammation

Project description:γδ T cells represent the primary innate source of IL-17 (γδT17) and are known to play a critical role in autoimmune and inflammatory diseases such as psoriasis. We here reported that psoriatic condition (IL-1b and IL-23) reshaped γδT17 cell metabolic signatures and promoted cytokine expression levels compared to homeostatic condition (IL-7). Acetyl-CoA carboxylase 1 (ACC1), a rate-limiting enzyme of fatty acid synthesis (FAS), directs the fate of IL-17-producing CD4 T cells (Th17) differentiation. However, little is known about the role of ACC1-mediated FAS in their innate IL-17-producer counterpart, γδT17 cells. We further investigated the role of FAS in γδT17 by comparing the effect of pharmacological inhibitor Soraphen A (SorA) on DMSO vehicle under psoriatic conditions (IL-1b and IL-23). Interestingly, ACC inhibition shifts the lipid metabolism in γδT17 cells, which allows them to cope with lipid demand without affecting cellular viability.

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Insights into the role of de novo fatty acid synthesis in IL-17-producing γδ T cells upon psoriatic inflammation

Project description:γδ T cells produce the primary innate source of IL-17 (γδT17) and are known to play a critical role in autoimmune and inflammatory diseases such as psoriasis. We here reported that psoriatic condition (IL-1b and IL-23) reshaped metabolic signatures and effector function of γδT17 cells compared to homeostatic condition (IL-7). Acetyl-CoA carboxylase 1 (ACC1), a rate-limiting enzyme of fatty acid synthesis (FAS), directs the fate of IL-17-producing CD4 T cells (Th17) differentiation. However, little is known about the role of ACC1-mediated FAS in their innate IL-17-producer counterpart, γδT17 cells. We further investigated the role of FAS in γδT17 by comparing the effect of pharmacological ACC inhibitor Soraphen A (SorA) on DMSO vehicle under psoriatic conditions (IL-1b and IL-23) to provide insights for clinical implication.

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Project description:Periodontitis (PD) is one of the most common human inflammatory diseases, yet the immunological mechanism linking oral and systemic immune responses are not well defined. Here, we show that the accumulation of interleukin-17 (IL-17)-producing γδT (γδT17) cells occurs not only in the oral cavity, but also in the peripheral lymph nodes and spleens in experimental periodontitis in mice. Strikingly, oral γδT17 cells derived from experimental periodontitis migrated to the inflamed joint and led to an exacerbation of rheumatoid arthritis (RA) in a collagen-induced arthritis model in mice. Mechansitically, we demonstrated that the dysbiosis in periodontitis led to an increase in production of complement component 3 (C3)-enriched extracellular vesicles (EVs) derived from macrophages. These C3-enriched EVs were taken up by γδT cells and stimulated intracellular C3a receptor to drive IL-17A production in γδT cells. Our findings revealed an previously unrecognized immunological mechanism linking periodontitis to RA through the accumulation and migration of oral γδT17 cells.

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