Methods to Study Neutrophil Extracellular Traps

TOPICAL COLLECTIONS

Guest Editor

Jyaysi Desai

Leiden University Medical Center

Dr. Jyaysi Desai is a postdoctoral researcher based in the Department of Rheumatology (lab of Professor R.E.M. Toes) at the Leiden University Medical Center. Her research focus is presently on understanding the role of neutrophils in driving autoimmune responses in different autoimmune diseases, such as rheumatoid arthritis. She is specifically interested in understanding the pathogenic role of neutrophil extracellular traps (NETs) in driving chronic inflammatory responses. Dr. Desai pursued her PhD in the lab of Professor H.J. Anders at the Ludwig-Maximillians University of Munich. During her PhD (2013-2017), she investigated how the crystals in different crystal-associated diseases elicit cytotoxicity of various immune and non-immune cells. Her research work showed that neutrophils, the first innate immune cells to get involved with crystals of monosodium urate (MSU), undergo a specific form of cell death to form neutrophil extracellular traps (NETs) in gouty arthritis. Since NETs are crucial players to induce inflammation in wide range of noninfectious and autoimmune diseases, Dr. Desai’s research about molecular insight of NET formation will help to specifically target NETs in various diseases to limit inflammation.

Collection Overview

Neutrophils are the most abundant immune cells present at the site of injury or inflammation. These cells, once activated by microbial or inflammatory triggers, can form neutrophil extracellular traps (NETs) by expelling their chromatin material in conjunction with several granular enzymes. Since their discovery in 2004, NETs have been identified as key players in a wide range of infectious and non-infectious diseases. They are believed to be crucially involved in the induction of inflammation. Although beneficial in the case of pathogens, NETs are thought to mediate detrimental effects in context of autoimmune diseases i.e. rheumatoid arthritis (RA), systematic lupus erythematosus (SLE) or ANCA-associated vasculitis (AAV). NETs may therefore serve as biomarkers as well as promising targets for future therapeutics of chronic inflammatory diseases. While cumulative evidence from in vitro, in vivo, and clinical diagnostics indicate the presence of NETs in pathophysiology of these diseases, the exact mechanisms how NETs contribute to autoimmunity and inflammation are still ill-defined.

This methods collection will focus on publishing the latest in vitro and in vivo methodologies to study NET formation and their implications in inflammatory diseases.