A5074357305- Immune Cell Function and Interaction
- CAR-T cell therapy research
- T-cell and B-cell Immunology
- Viral Infectious Diseases and Gene Expression in Insects
- Autophagy in Disease and Therapy
- Cancer Research and Treatments
- Dermatology and Skin Diseases
- Asthma and respiratory diseases
- Pancreatic function and diabetes
- Cytomegalovirus and herpesvirus research
- Transgenic Plants and Applications
- Nanowire Synthesis and Applications
- Epigenetics and DNA Methylation
- Silicon Carbide Semiconductor Technologies
- RNA modifications and cancer
Memorial Sloan Kettering Cancer Center
2019-2022
Novartis (United States)
2016-2021
Infection triggers expansion and effector differentiation of T cells specific for microbial antigens in association with metabolic reprograming. We found that the glycolytic enzyme lactate dehydrogenase A (LDHA) is induced CD8+ through phosphoinositide 3-kinase (PI3K) signaling. In turn, ablation LDHA inhibits PI3K-dependent phosphorylation Akt its transcription factor target Foxo1, causing defective antimicrobial immunity. deficiency cripples cellular redox control diminishes adenosine...
Abstract Infection triggers clonal expansion and effector differentiation of microbial antigen-specific T cells in association with metabolic reprograming. Here, we show that the glycolytic enzyme lactate dehydrogenase A (LDHA) is induced CD8 + via phosphoinositide 3-kinase (PI3K)-dependent mechanisms. In turn, ablation LDHA inhibits PI3K-dependent phosphorylation Akt its transcription factor target Foxo1, causing defective antimicrobial immunity. deficiency cripples cellular redox control...