LMP student seminars: 24 September
Each week during term time, MSc and PhD candidates in the Department of Laboratory Medicine and Pathobiology present their research.
Anyone is welcome. No need to register.
Location: Medical Sciences Building, rooms 4171 or 4279, see below.
As part of the core research curriculum, students taking LMP1001/2/3: Graduate Seminars in Laboratory Medicine and Pathobiology will present their projects. Please see abstracts below.
Group 1: Brain and Neuroscience
Location: MSB 4171
Jarryll Uy
- Title: TBA
- Supervisor: TBA
Ann Mansur
- Title: TBA
- Supervisor: TBA
Group 5: Infectious Diseases, Inflammation and Immunology
Location: MSB 4279
Veronica Chang
- Title: TBA
- Supervisor: TBA
Maya Allen
- Title: Unbiased and Spatial Proteomics of Kidney Allograft Biopsies: Terminal Complement Proteins Dominate Chronic Active Antibody Mediated Rejection
- Supervisors: Dr. Ana Konvalinka
Abstracts
Maya Allen: Unbiased and Spatial Proteomics of Kidney Allograft Biopsies: Terminal Complement Proteins Dominate Chronic Active Antibody Mediated Rejection
Transplantation is the optimal treatment for end-stage kidney disease, but many grafts fail due to antibody mediated rejection (AMR). AMR is caused by donor-specific antibodies (DSA) against antigens on the graft endothelium. Diagnostic criteria for AMR in kidney allografts consider graft injury, evidence for antibody interaction with the endothelium (i.e. C4d staining in the microvasculature), and circulating DSA. AMR is further stratified into active (aAMR) or chronic-active (caAMR) by the presence of chronic glomerulopathy in the latter. Intriguingly, 50% of patients exhibiting microvascular inflammation consistent with AMR do not have DSA (DSA-AMR). To gain insights into the molecular underpinnings of AMR with and without DSA, we investigated proteomic differences in for-cause biopsies of these groups. Laser capture microdissection was used to separate tubulointerstitium and glomeruli of biopsies from 83 DSA+ and DSA- patients with aAMR or caAMR, followed by unbiased proteomic analysis using a Q-Exactive HFX mass spectrometer. Complement cascade proteins were amongst the most significantly differentially expressed proteins in both compartments. In the tubulointerstitium, terminal complement components were increased in DSA+AMR compared to DSA-AMR, and in caAMR compared to aAMR. In the glomeruli, all quantified complement proteins were increased in caAMR compared to aAMR, with no significant difference between DSA+AMR and DSA-AMR biopsies. Preliminary imaging mass cytometry data demonstrated C5a expression in the basement membranes of biopsies with DSA+caAMR, while C5b-9 co-stained with IgG. Increased complement expression in both DSA+ and DSA- biopsies with caAMR, with C5a expression notable in basement membranes, suggests complement involvement in chronic glomerulopathy.
Contact
No need to register.
Contact lmp.grad@utoronto.ca with any questions.