Publications by authors named "B Becher"

Group 1 innate lymphoid cells (ILCs) encompass NK cells and ILC1s, which have non-redundant roles in host protection against pathogens and cancer. Despite their circulating nature, NK cells can establish residency in selected tissues during ontogeny, forming a distinct functional subset. The mechanisms that initiate, maintain, and regulate the conversion of NK cells into tissue-resident NK (trNK) cells are currently not well understood.

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  • Tumor-associated neutrophils (TANs) vary in function depending on the type of cancer, with their role being more significant in metabolic dysfunction-related liver cancer than in viral-related liver cancer.* -
  • In metabolic dysfunction-associated hepatocellular carcinoma (MASH-related HCC), specific TANs (SiglecFhi) promote tumor growth and immune evasion by enhancing stemness and inhibiting the immune response.* -
  • Targeting SiglecFhi TANs can improve the effectiveness of immunotherapy, as their removal increases cancer cell recognition and correlates with poor patient outcomes due to resistance to treatment.*
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  • Cytokines like IL-4 activate immune cell responses by triggering transcription factors, specifically STAT6, which affects cellular functions and metabolism.* -
  • The aryl hydrocarbon receptor (AhR) plays a regulatory role by enhancing certain IL-4 responses and inhibiting the metabolic shift towards fatty acid β-oxidation.* -
  • AhR influences the activity of SHP-1, extending STAT6's effect on target genes, suggesting that AhR's role in this process may operate through a nongenomic mechanism.*
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A healthy mammalian central nervous system (CNS) harbors a diverse population of leukocytes including members of the mononuclear phagocyte system (MPS). Exerting their specific functions, CNS tissue-resident macrophages as well as associated monocytes and dendritic cells (DCs) maintain CNS homeostasis. Under neuroinflammatory conditions, leukocytes from the systemic immune compartment invade the CNS.

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In neuroinflammatory diseases, systemic (blood-borne) leukocytes invade the central nervous system (CNS) and lead to tissue damage. A causal relationship between neuroinflammatory diseases and dysregulated cytokine networks is well established across several preclinical models. Cytokine dysregulation is also observed as an inadvertent effect of cancer immunotherapy, where it often leads to neuroinflammation.

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