Jasmine Nour (Italy)
University of Milan Department of Pharmacological and Biomolecular SciencesAuthor Of 2 Presentations
Live Q&A (ID 1550)
O004 - Role of the Interleukin-1 Receptor/Toll Like Receptor TIR8/SIGIRR in experimental atherosclerosis (ID 1235)
Abstract
Background and Aims
TIR8/SIGIRR dampens the excessive activation mediated by ILRs and TLRs agonism and thus is a key regulator of inflammation. Aim of this study was to investigate the role of TIR8 in atherosclerosis.
Methods
8 weeks old-LDLR KO and TIR8/LDLR double KO (DKO) male mice were fed with standard diet (STD) or cholesterol-enriched diet (WTD) for 12 weeks. Plasma lipid profiling, extensive immunophenotyping and histological analysis of the atherosclerotic plaques were then performed.
Results
TIR8 deletion in STD-fed LDLR KO mice impacts circulating immune cell profile: decreased percentage of T lymphocytes (-29%, p<0.001) and increased percentage of B cells (+14%, p<0.05) were observed compared to LDLR KO mice, as well as increased mature Natural Killer cells (+13%, p<0.0001), as already described in the TIR8 KO mouse model. When fed a cholesterol rich diet for 12 weeks to induce atherosclerosis, in addition to changes observed on STD, also circulating levels of monocytes increased in DKO mice compared to LDL-R KO mice (mean 1464 vs 910 cells/ul, p<0.05). These changes in immune profile, however, did not affect atherosclerotic plaque area or stability. Similarly, no differences in plasma lipid profile were observed.
Conclusions
TIR8 deficiency in LDLR KO mice increases NKs and monocytes blood levels compared to LDL-R KO mice. Changes in these immune subsets, however, do not impact the development of atherosclerosis.
Presenter of 2 Presentations
Live Q&A (ID 1550)
O004 - Role of the Interleukin-1 Receptor/Toll Like Receptor TIR8/SIGIRR in experimental atherosclerosis (ID 1235)
Abstract
Background and Aims
TIR8/SIGIRR dampens the excessive activation mediated by ILRs and TLRs agonism and thus is a key regulator of inflammation. Aim of this study was to investigate the role of TIR8 in atherosclerosis.
Methods
8 weeks old-LDLR KO and TIR8/LDLR double KO (DKO) male mice were fed with standard diet (STD) or cholesterol-enriched diet (WTD) for 12 weeks. Plasma lipid profiling, extensive immunophenotyping and histological analysis of the atherosclerotic plaques were then performed.
Results
TIR8 deletion in STD-fed LDLR KO mice impacts circulating immune cell profile: decreased percentage of T lymphocytes (-29%, p<0.001) and increased percentage of B cells (+14%, p<0.05) were observed compared to LDLR KO mice, as well as increased mature Natural Killer cells (+13%, p<0.0001), as already described in the TIR8 KO mouse model. When fed a cholesterol rich diet for 12 weeks to induce atherosclerosis, in addition to changes observed on STD, also circulating levels of monocytes increased in DKO mice compared to LDL-R KO mice (mean 1464 vs 910 cells/ul, p<0.05). These changes in immune profile, however, did not affect atherosclerotic plaque area or stability. Similarly, no differences in plasma lipid profile were observed.
Conclusions
TIR8 deficiency in LDLR KO mice increases NKs and monocytes blood levels compared to LDL-R KO mice. Changes in these immune subsets, however, do not impact the development of atherosclerosis.