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- W4313373531 abstract "Abstract Genome wide association studies (GWAS) identified several single nucleotide polymorphisms (SNPs) in inflammatory diseases. However, it is difficult to determine the gene that GWAS identified SNPs affect and in which cell type(s). RNA-seq analysis of immune cells from 89 healthy humans, led to the identification of the gene laccase domain containing 1 (LACC1), as one of the most promising targets for investigating the role of human gene polymorphisms in inflammatory bowel disease (IBD). LACC1 is a critical immunometabolic mediator in macrophages that drives fatty-acid oxidation. Surprisingly, we found that polymorphisms near LACC1 that have been linked to IBD correlated with significantly lower LACC1 expression in naïve and activated CD4 and CD8 T cells. No difference in expression was observed in macrophages, where it’s highly expressed and has been shown to influence macrophage function. Thus, we hypothesized that these polymorphisms contribute to the genetic risk for IBD by reducing LACC1 expression and, subsequently, inducing T cell dysfunction. As LACC1 plays an important role in macrophage fatty acid metabolism, we tested if this held true in T cells. In our study, knockdown of LACC1 in human CD4 T cells increased mitochondrial mass and lipid droplet formation. This change in metabolism was associated with a significantly reduced production of several cytokines, including IL-2 and IFNg, following anti-CD3/CD28 stimulation. Further, levels of expression of the T cell activation marker CD25 were also attenuated. In summary, our studies provide insights into new mechanisms controlling T cell metabolism and suggest that LACC1 may provide a target for regulating T cell function to prevent inflammatory and autoimmune diseases." @default.
- W4313373531 created "2023-01-06" @default.
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- W4313373531 date "2020-05-01" @default.
- W4313373531 modified "2023-09-27" @default.
- W4313373531 title "Connecting metabolism to inflammation: the role of <i>LACC1</i> in inflammatory diseases" @default.
- W4313373531 doi "https://doi.org/10.4049/jimmunol.204.supp.224.37" @default.
- W4313373531 hasPublicationYear "2020" @default.
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