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

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 with intratracheally to establish a model of pulmonary aspergillosis. For analysis, neutrophils were purified from the bone marrow and incubated with hyphae.

Results: Mice lacking Dcir exhibited improved clearance of from 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 of hyphae, attributed to higher degranulatory activity, triggered by intracellular Ca mobilization.

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.