Human T9 cells rely on PPAR-γ-mediated cystine uptake to prevent lipid peroxidation and bioenergetic failure.

T9 cells are implicated in allergic skin inflammation and depend on the transcription factor PPAR-γ for full effector function. In this study, we uncovered a role for PPAR-γ in the amino acid metabolism of human T9 cells. In in-vitro-primed T9 cells, PPAR-γ expression positively correlated with the expression of SLC7A8, which encodes LAT2, a transporter of large neutral amino acids, including cystine.

IL-9 sensitizes human T2 cells to proinflammatory IL-18 signals in atopic dermatitis.

Background: T2 cells crucially contribute to the pathogenesis of atopic dermatitis (AD) by secreting high levels of IL-13 and IL-22. Yet the upstream regulators that activate T2 cells in AD skin remain unclear. IL-18 is a putative upstream regulator of T2 cells because it is implicated in AD pathogenesis and has the capacity to activate T cells.

PPAR-γ regulates the effector function of human T helper 9 cells by promoting glycolysis.

T helper 9 (T9) cells promote allergic tissue inflammation and express the type 2 cytokines, IL-9 and IL-13, as well as the transcription factor, PPAR-γ. However, the functional role of PPAR-γ in human T9 cells remains unknown. Here, we demonstrate that PPAR-γ drives activation-induced glycolysis, which, in turn, promotes the expression of IL-9, but not IL-13, in an mTORC1-dependent manner.

The Concept of Pathogenic TH2 Cells: Collegium Internationale Allergologicum Update 2021.

T helper (TH) cells have evolved into distinct subsets that mediate specific immune responses to protect the host against a myriad of infectious and noninfectious challenges. However, if dysregulated, TH-cell subsets can cause inflammatory disease. Emerging evidence now suggests that human allergic disease is caused by a distinct subpopulation of pathogenic TH2 cells.

Targeting T Cell Metabolism in Inflammatory Skin Disease.

A properly functioning T cell compartment is crucial to protect the host from infections, tumors, and environmental substances. In recent years, it has become increasingly clear that the processes underlying proper T cell activation, proliferation, and differentiation require well-tuned and dynamic changes in T cell metabolism. Thus, proper metabolic reprogramming in T cells is crucial to ensure proper immunity in the context of infection and anti-tumor immunity.

Transcriptomic analysis reveals reduced transcriptional activity in the malaria parasite during progression into dormancy.

Relapses of dormant liver hypnozoites compromise malaria eradication efforts. New radical cure drugs are urgently needed, yet the vast gap in knowledge of hypnozoite biology impedes drug discovery. We previously unraveled the transcriptome of 6 to 7 day-old liver stages, highlighting pathways associated with hypnozoite dormancy (Voorberg-van der Wel et al.

Monitoring of genetically modified Escherichia coli in laboratory wastewater.

Containment of genetically modified (GM) microorganisms such as Escherichia coli is a legal requirement to protect the environment from an unintended release and to avoid horizontal gene transfer (HGT) of recombinant DNA to native bacteria. In this study, we sampled the laboratory wastewater (LWW) at a large Swiss university from three sources over 2 years and cultured ampicillin-resistant, presumptive GM E. coli.

Malaria parasites possess a telomere repeat-binding protein that shares ancestry with transcription factor IIIA.

Telomere repeat-binding factors (TRFs) are essential components of the molecular machinery that regulates telomere function. TRFs are widely conserved across eukaryotes and bind duplex telomere repeats via a characteristic MYB-type domain. Here, we identified the telomere repeat-binding protein PfTRZ in the malaria parasite Plasmodium falciparum, a member of the Alveolate phylum for which TRFs have not been described so far.

Heterochromatin protein 1 secures survival and transmission of malaria parasites.

Clonally variant expression of surface antigens allows the malaria parasite Plasmodium falciparum to evade immune recognition during blood stage infection and secure malaria transmission. We demonstrate that heterochromatin protein 1 (HP1), an evolutionary conserved regulator of heritable gene silencing, controls expression of numerous P. falciparum virulence genes as well as differentiation into the sexual forms that transmit to mosquitoes.