Electric Literature of C13H20N4O2. The reaction of aromatic heterocyclic molecules with protons is called protonation. Aromatic heterocycles are more basic than benzene due to the participation of heteroatoms. Compound: 1-Hexyl-3,7-dimethyl-1H-purine-2,6(3H,7H)-dione, is researched, Molecular C13H20N4O2, CAS is 1028-33-7, about Acute cellular rejection in small-bowel transplantation impairs NCR+ innate lymphoid cell subpopulation 3/interleukin 22 axis. Author is Pucci Molineris, Melisa; Gonzalez Polo, Virginia; Rumbo, Carolina; Fuxman, Claudia; Lowestein, Carlos; Nachman, Fabio; Rumbo, Martin; Gondolesi, Gabriel; Meier, Dominik.
Acute cellular rejection (ACR) remains as one of the main causes of graft loss and death in intestinal transplant (ITx) patients. ACR promotes intestinal injury, disruption of the mucosal barrier, bacterial translocation, and organ dysfunction. As epithelial regeneration is critical in reversing these consequences, the functional axis between the innate lymphoid cell subpopulation 3 (ILC3) and interleukin 22 plays an essential role in that process. Natural-cytotoxic-receptor-pos. (NCR+) ILC3 cells have been demonstrated to induce intestinal-stem-cell proliferation along with an IL-22-dependent expansion of that population in several intestinal pathologies, though thus far not after ITx. Therefore, we intended to determine the impact of chronic immunosuppression and ACR on ILC3 cells and interleukin-22 (IL-22) production in the lamina propria after that intervention. We compared biopsies from healthy volunteers with biopsies from ITx recipients without or with mild-to-moderate ACR, using flow cytometry and the quant.-PCR. NCR+ ILC3 cells were found to be unaffected by immunosuppression at different time points posttransplant when patients did not experience ACR, but were diminished upon the occurrence of ACR independently of the post-ITx time. Moreover, IL-22-expression levels were notably reduced in ACR. The NCR+-ILC3/IL-22 axis is impaired during ACR contributing to a delay in or lack of a complete and efficient epithelial regeneration.
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Reference:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem