@article{LuuSchuetzLauthetal.2023,
  author    = {Luu, Maik and Sch{\"u}tz, Burkhard and Lauth, Matthias and Visekruna, Alexander},
  title     = {The impact of gut microbiota-derived metabolites on the tumor immune microenvironment},
  series = {Cancers},
  volume    = {15},
  journal   = {Cancers},
  number    = {5},
  issn      = {2072-6694},
  doi       = {10.3390/cancers15051588},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-311005},
  year      = {2023},
  abstract  = {Prevention of the effectiveness of anti-tumor immune responses is one of the canonical cancer hallmarks. The competition for crucial nutrients within the tumor microenvironment (TME) between cancer cells and immune cells creates a complex interplay characterized by metabolic deprivation. Extensive efforts have recently been made to understand better the dynamic interactions between cancer cells and surrounding immune cells. Paradoxically, both cancer cells and activated T cells are metabolically dependent on glycolysis, even in the presence of oxygen, a metabolic process known as the Warburg effect. The intestinal microbial community delivers various types of small molecules that can potentially augment the functional capabilities of the host immune system. Currently, several studies are trying to explore the complex functional relationship between the metabolites secreted by the human microbiome and anti-tumor immunity. Recently, it has been shown that a diverse array of commensal bacteria synthetizes bioactive molecules that enhance the efficacy of cancer immunotherapy, including immune checkpoint inhibitor (ICI) treatment and adoptive cell therapy with chimeric antigen receptor (CAR) T cells. In this review, we highlight the importance of commensal bacteria, particularly of the gut microbiota-derived metabolites that are capable of shaping metabolic, transcriptional and epigenetic processes within the TME in a therapeutically meaningful way.},
  language  = {en}
}
@article{BrosinskyLeisterChengetal.2022,
  author    = {Brosinsky, Paulin and Leister, Hanna and Cheng, Nan and Varelas, Xaralabos and Visekruna, Alexander and Luu, Maik},
  title     = {Verteporfin protects against Th17 cell-mediated EAE independently of YAP inhibition},
  series = {European Journal of Immunology},
  volume    = {52},
  journal   = {European Journal of Immunology},
  number    = {9},
  doi       = {10.1002/eji.202149564},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-287234},
  pages     = {1523 -- 1526},
  year      = {2022},
  abstract  = {The known YAP inhibitor verteporfin is capable of repressing IL-17A production in Th17 cells. However, this effect is mediated independently of YAP and can ameliorate Th17-mediated experimental autoimmune encephalomyelitis (EAE) upon in vivo administration. The data suggest verteprofin's mode of action for the design of novel therapeutic autoimmune disease intervention.},
  language  = {en}
}