LAIR-1 Limits Neutrophilic Airway Inflammation

In conclusion, the immune inhibitory receptor LAIR-1 suppresses neutrophil tissue migration and acts as a negative regulator of neutrophil-driven airway inflammation during lung diseases. Following our recent observations in humans, this study provides crucial in-vivo evidence that LAIR-1 is a promising target for pharmacological intervention in such pathologies. Introduction The lungs are constantly exposed to potential pathogens and other harmful agents. To protect against sudden incursions, neutrophils patrol the lung capillaries. A rapid and robust neutrophil response is crucial to antimicrobial defense (1, 2). Neutrophilic inflammation is a common trait of some respiratory diseases. We have recently reviewed literature showing that due to the promiscuous cytotoxicity of neutrophils, excessive neutrophilic inflammation induces immune injury in viral infection (3). Therefore, balancing pathogen eradication with neutrophil-induced tissue injury is of the utmost importance to preserve tissue homeostasis. However, the mechanisms that regulate neutrophilic inflammation in the airways are still unclear. Leukocyte-associated Ig-like receptor (LAIR)-1, also known as CD305, is an ITIM-bearing inhibitory receptor expressed on majority of immune cells (4). Mouse and human LAIR-1 share ~40% homology, potent inhibitory capacity and bind to collagen and collagen-like molecules (5–8). Circulating neutrophils do not express LAIR-1 on the cell surface, but surface e...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research