Targeting CRAC channels in inflammatory bowel disease.
Sven KappelChristine PeineltPublished in: EMBO molecular medicine (2022)
Inflammatory bowel disease (IBD) is a collective term for inflammatory diseases of the human gastrointestinal (GI) tract that are characterized by perturbations in the intestinal immune responses. In their study, Letizia et al (2022) found an enrichment of CD4 + effector T cells, interferon gamma (IFNγ) producing CD8 + T cells, regulatory T cells, and innate lymphoid cells (ILC) in the lamina propria (LP) of IBD patients. In these cells, pharmacological inhibition of store-operated calcium entry (SOCE) reduced cytokine production. In addition, in a murine IBD model, systemic SOCE inhibition reduced IBD severity and weight loss.
Keyphrases
- regulatory t cells
- dendritic cells
- induced apoptosis
- immune response
- weight loss
- cell cycle arrest
- end stage renal disease
- ulcerative colitis
- endothelial cells
- ejection fraction
- chronic kidney disease
- newly diagnosed
- bariatric surgery
- oxidative stress
- cell death
- endoplasmic reticulum stress
- signaling pathway
- body mass index
- preterm infants
- adipose tissue
- cancer therapy
- toll like receptor
- cell proliferation
- gastric bypass
- preterm birth
- patient reported outcomes
- gestational age