Differential dependencies of monocytes and neutrophils on dectin-1, dectin-2 and complement for the recognition of fungal particles in inflammation.
We have re-investigated the role of the complement system and the non-opsonic pattern recognition receptors dectin-1 and dectin-2 in the recognition of fungal particles by inflammatory neutrophils, monocytes and macrophages. We have used in vivo and ex vivo models to study the recognition and response of these cells: i) We confirm previous observations regarding the importance of complement to neutrophil but not monocytic responses; ii) We show that dectin-1 is important for driving inflammatory cell recruitment to fungal stimuli and that it biases the immediate inflammatory response to one that favors neutrophil over monocyte recruitment; iii) We show that dectin-2 contributes to the physical recognition of fungal particles by inflammatory monocytes/macrophages, but is also expressed on neutrophils, where we show it has the potential to contribute to cellular activation; iv) Additionally, we show that serum-opsonization has the potential to interfere with non-opsonic recognition of fungal particles by dectin-1 and dectin-2, presumably through masking of ligands. Collectively these roles are consistent with previously described roles of dectin-1 and dectin-2 in driving inflammatory and adaptive immune responses and complement in containing fungal burdens. This study emphasizes the importance of heterogeneity of receptor expression across myeloid cell subsets in protective immune responses.
Institute of Infection and Immunity, Cardiff University School of Medicine, Cardiff, United Kingdom.
Jacqueline U
JU
McDonald
Marcela
M
Rosas
Gordon D
GD
Brown
Simon A
SA
Jones
Philip R
PR
Taylor
D000818:Animals; D003165:Complement System Proteins; D005434:Flow Cytometry / Q000379:methods; D005786:Gene Expression Regulation; D007107:Immune System; D007249:Inflammation / Q000378:metabolism*; D037181:Lectins, C-Type / Q000096:biosynthesis*; D008024:Ligands; D051379:Mice; D009000:Monocytes / Q000382:microbiology*; D009181:Mycoses / Q000382:microbiology* / Q000473:pathology; D041681:NIH 3T3 Cells; D009504:Neutrophils / Q000378:metabolism / Q000382:microbiology*; D009895:Opsonin Proteins / Q000378:metabolism; D010641:Phenotype; D000099181:Dectin-1
D003165:Complement System Proteins; D037181:Lectins, C-Type; D008024:Ligands; D009895:Opsonin Proteins; D000099181:Dectin-1; C445340:dectin-2, mouse