L2pB1 cells are a subset of B-1 B lymphocytes expressing programmed death ligand 2 (PD-L2) on their surface. They constitute 30-50% of B lymphocytes in the mouse peritoneal cavity and contribute to the production of natural IgM antibody. Previous studies have indicated a protective role of B-1 B cells in attenuating atherosclerosis and insulin resistance. We report that L2pB1 cells possess a unique IgM antibody specificity for phosphorylcholine (PC) and phosphatidylcholine (PtC) IgM enabling them to perform PC- and PtC-specific phagocytosis of PtC-nanoparticles. Here we demonstrate that induced depletion of L2pB1 in a transgenic mouse model with L2pB1-specific diphtheria toxin receptor (DTR) expression increases abdominal inflammation in the peritoneal cavity as well as the visceral adipose tissue in diet-induced obese (DIO) mice. L2pB1-depleted DIO mice also display increased triglycerides and blood glucose levels per gram of body weight relative to PBS-injected control DIO mice. Our results suggest that L2pB1 cells may play a role in anti-inflammatory regulation in DIO. Further investigation is required to discover how L2pB1 cells protect from obesity-induced inflammation and whether L2pB1 cells can provide cellular therapy to control chronic inflammation in obese patients. / 2018-06-16T00:00:00Z
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/16760 |
| Date | 17 June 2016 |
| Creators | Newmark, Jordan Alison |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
| Rights | Attribution-NonCommercial 4.0 International, http://creativecommons.org/licenses/by-nc/4.0/ |
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