Glucose-dependent insulinotropic polypeptide receptor signaling alleviates gut inflammation in mice.

Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are gut-derived peptide hormones that potentiate glucose-dependent insulin secretion. The clinical development of GIP receptor (GIPR)-GLP-1 receptor (GLP-1R) multi-agonists exemplified by tirzepatide and emerging GIPR antagonist-GLP-1R agonist therapeutics such as maritide is increasing interest in the extra-pancreatic actions of incretin therapies. Both GLP-1 and GIP modulate inflammation, with GLP-1 also acting locally to alleviate gut inflammation in part through anti-inflammatory actions on GLP-1R+ intestinal intraepithelial lymphocytes.

Cytofluorometric analysis of the maturation and activation of bone marrow-derived dendritic cells to assess immunogenic cell death.

Immunogenic cell death (ICD) has emerged as a pivotal form of cell death in anti-cancer therapy as it combines the ability to both eliminate cancer cells and simultaneously activate anti-tumor immunity, thereby contributing to the establishment of long-term immunological memory. Antigen-presenting cells (APCs), with an emphasis on dendritic cells (DCs), play a central role in bridging the innate and adaptive immune systems. DCs recognize and present antigens derived from the dying cancer cells to T cells in the lymph nodes, resulting in T cell activation.

CX3CL1 release during immunogenic apoptosis is associated with enhanced anti-tumour immunity.

Introduction: Immunogenic cell death (ICD) has emerged as a novel option for cancer immunotherapy. The key determinants of ICD encompass antigenicity (the presence of antigens) and adjuvanticity, which involves the release of damage-associated molecular patterns (DAMPs) and various cytokines and chemokines. CX3CL1, also known as neurotactin or fractalkine, is a chemokine involved in cellular signalling and immune cell interactions.