Abstract
Central nervous system (CNS) microglia (MG) and peripheral tissue macrophages (MO) remove pathogens by phagocytosis. Zymosan, a model yeast pathogen, is a β-glucan rich particle that readily activates the complement system and then becomes C3bi-opsonized (op). Complement receptor-3 (CR3) has initially been implicated in mediating the phagocytosis of both C3bi-op and non-opsonized (nop) zymosan by MO through C3bi and β-glucan binding sites, respectively. Later, the role of CR3 as a phagocytic b-glucan receptor has been questioned and the supremacy of β-glucan receptor Dectin-1 advocated. We compare here between primary mouse CNS MG and peripheral tissue MO with respect to CR3 and Dectin-1 mediated phagocytosis of C3biop and nop zymosan. We report that MG and MO display similar as well as dissimilar functional properties in this respect. Although CR3 and Dectin-1 function both as b-glucan/ non-opsonic receptors in MG during nop zymosan phagocytosis, Dectin-1, but not CR3, does so in MO. CR3 functions also as a C3bi/opsonic receptor in MG and MO during C3bi-op zymosan phagocytosis, leading to phagocytosis which is more efficient than that of nop zymosan. Dectin-1 contributes, albeit less than CR3, to phagocytosis of C3bi-op zymosan in MG and further less in MO, suggesting that C3bi-opsonization does not block all β-glucan sites on zymosan from binding Dectin-1 on phagocytes. Thus, altogether CR3 and Dectin-1 contribute both to phagocytosis of nop and C3bi-op zymosan in MG, whereas MO switch from CR3-independent/Dectin-1- dependent phagocytosis of nop zymosan to phagocytosis of C3bi-op zymosan where CR3 dominates over Dectin-1.
Original language | English |
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Pages (from-to) | 823-830 |
Number of pages | 8 |
Journal | GLIA |
Volume | 58 |
Issue number | 7 |
DOIs | |
State | Published - May 2010 |
Keywords
- αM/β2
- β-glucan
- CD11b/CD18
- Dectin-1
- Integrin
- Zymosan