The C-type lectin receptor Dcir () restrainselimination by limiting the degranulatory activity of neutrophils.

Abstract

INTRODUCTION: C-type lectin receptors (CLRs) are innate sensors crucial for antifungal and antimycobacterial responses, contributing to host defenses against pathogens, including the ubiquitous mold. Dendritic cell immunoreceptor (Dcir) modulates immune responses by limiting the development of inflammation and autoimmunity; however, its involvement in fungal infections has not been previously established. METHODS: Wild-type and Dcir-knockout C57BL/6J mice were infected withintratracheally to establish a model of pulmonary aspergillosis. Foranalysis, neutrophils were purified from the bone marrow and incubated withhyphae. RESULTS: Mice lacking Dcir exhibited improved clearance offrom the lungs, while tissue inflammation-assessed by phagocyte recruitment and inflammatory cytokine levels within the lungs-did not change significantly compared to Dcir competent mice. Neutrophils from Dcir-deficient mice exhibited enhanced killing ofhyphae, attributed to higher degranulatory activity, triggered by intracellular Camobilization. DISCUSSION: The results indicate a potential association between Dcir and downregulation of signalling pathways associated with neutrophil exocytosis. Thus, Dcir is a potential novel fungal sensor that, unlike other CLR family members, primarily fine-tunes host effector responses.