Nidhi Kaza
Research Mentor: Jason Knight
Mentor Department: Internal Medicine/Rheumatology, Medicine
Author(s): Not Available
Session: Session 3 (11:00 AM – 11:50 AM)
Presentation Type: Poster 74
Abstract
Antiphospholipid syndrome (APS) is a systemic autoimmune disease in which the patient’s immune system produces disease-defining antiphospholipid antibodies (aPL) that attack their own body, clinically leading to recurrent thrombotic events and/or pregnancy morbidity of patients This study focuses on the profiling of B lymphocytes (B cells), from patients’ Peripheral Blood Mononuclear Cells (PBMCs). B-cells are a type of white blood cell that make infection-fighting proteins called antibodies. There are different isotypes of these antibodies, such as IgG, IgM, and IgA. Diagnosing APS relies heavily on serologic detection of anti-ß2-glycoprotein I (ß2GPI) antibodies, particularly the IgG and IgM isotypes, a concept that is based on consensus guidelines. Pathogenic anti-ß2GPI antibodies are the defining serologic feature of APS, yet the origins and activation states of the B cells that produce them remain incompletely understood. Patients were grouped based on their anti-ß2GPI antibody isotypes, identified via Enzyme-Linked Immunosorbent Assay (ELISA). Three groups were established according to plasma anti-ß2GPI levels: isolated IgG (SGU > 20), isolated IgM (SMU > 20), and negative (SGU, SMU, and SAU all < 20). PBMCs from patients and healthy donors were isolated from whole blood, counted, and cryopreserved in liquid nitrogen. Once all samples were collected, thawed PBMCs were profiled using spectral flow cytometry to identify B-cell subsets, including Transitional, Naive, Memory, Follicular (FO) and Marginal Zone (MZ) B cells.
