Understanding Plasma Cell Differentiation in SLE
Abstract
Our immune system functions to eradicate pathogens from our body. One arm of this defense is through antibodies which facilitate pathogen clearance. However, if antibodies target our own body, autoimmune diseases, such as Systemic Lupus Erythematosus (SLE), can arise. Most SLE patients have anti-nuclear antibodies (ANA). These antibodies recognize an array of molecules that normally reside in the nucleus of cells. However, when an injury or infection occurs, these molecules can be released from the nucleus of dying cells, thereby becoming accessible to binding by ANA, which usually results in an inflammatory response. Plasma cells are the immune cells that produce antibodies, and they can arise from B cells through different pathways. Our previous results have shown that the differentiation of most ANA+B cells to plasma cells is prevented in healthy individuals, a process we call tolerance. In SLE, this tolerance process is unsuccessful, thereby leading to secretion of ANA and to subsequent inflammatory reactions throughout the body. Our previous research has shown that SLE patients can be separated in two groups based on their pattern of ANA+ plasma cells. In the proposed project, we aim to study the pathways that lead to the emergence of ANA+ plasma cells in SLE. Included among ANA+PCs are cells making anti-DNA and anti-Sm antibodies, both of which are known to contribute to disease in SLE. We will compare the two groups of patients; we hypothesize that each group has a distinct pathway for the development of ANA+ plasma cells. Moreover, we will determine how to cause the differentiation of a naive or memory ANA+ cells to PCs to provide insights into prevention.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 2022
- Accession Number
- AD1191329
Entities
People
- Betty Diamond
Organizations
- The Feinstein Institute for Medical Research