Role of neutrophils in systemic autoimmune diseases

Mariana J Kaplan

doi:10.1186/ar4325

Abstract

Neutrophils have emerged as important regulators of innate and adaptive immune responses. Recent evidence indicates that neutrophils display marked abnormalities in phenotype and function in various systemic autoimmune diseases, and may play a central role in initiation and perpetuation of aberrant immune responses and organ damage in these conditions. This review discusses the putative roles that neutrophils and aberrant neutrophil cell death play in the pathogenesis of various systemic autoimmune diseases, including systemic lupus erythematosus, small vessel vasculitis and rheumatoid arthritis.

Highlights

Neutrophils, terminally differentiated cells with a short lifespan in circulation, are the most abundant leukocytes in the human body, with homeostasis maintained by their continuous release from the bone marrow
Upon homing to inflamed tissues, neutrophils engage in complex bidirectional interactions with macrophages, dendritic cells (DCs), natural killer cells, lymphocytes and mesenchymal stem cells, thereby influencing innate and adaptive immune responses [5,6]
Summary and conclusions Neutrophils have emerged as important regulators of innate and adaptive immune responses, display marked abnormalities in phenotype and function in various systemic autoimmune diseases, and may play a central role in initiation and perpetuation of aberrant immune responses and organ damage in these conditions

Summary

Introduction

Neutrophils, terminally differentiated cells with a short lifespan in circulation, are the most abundant leukocytes in the human body, with homeostasis maintained by their continuous release from the bone marrow. This review highlights the putative roles that neutrophils and aberrant neutrophil cell death play in several of these diseases, including systemic vasculitides, systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). NETosis results in elevated levels of PR3 and MPO that are contained in the NETs. Further, circulating MPO– DNA complexes have been detected in patients with AASV, suggesting that NET formation triggers vascular inflammation and promotes autoimmune responses against neutrophil components in these diseases [49].

Results

Conclusion