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. 2019 Mar 29;9:75. doi: 10.3389/fcimb.2019.00075

Table 1.

Classification of currently described human Fcγ Receptors, and evidences of their role in hRSV-induced pathogenesis.

Type Receptor Alternative name/CD Main function Evidence after hRSV infection Suggested role References indicating a role during hRSV infection
Classical FcγRs (Recognize ICs on the cell surface) FcγRI CD64 Activating a
FcγRIIa CD32a Activating
FcγRIIb CD32b Inhibitory
FcγRIIc CD32c Activating
FcγRIIIa CD16a Activating Increased presence of FcγRIIIA+ NK cells, and lung damage in patients with severe hRSV infections The expression of FcγRIIIA on NK cells negatively influences the immune response during hRSV infection Tripp et al., 2002
FcγRIIIb CD16b Activating
Non-classical FcγRs (C-type lectins that recognize ICs on cell surface or non-classic FcγRs that recognize ICs inside the cell) CD23 CD23
DC-SIGN CD209 Recognition of glycans through a carbohydrate recognition domain (CRD) In vitro: mAb-blockade of DC-SIGN increases human DC maturation markers (CD80, CD86) after hRSV infection. hRSV-DC interaction through DC-SIGN might impair DC maturation Johnson et al., 2012
FcRn Control of endosomal routing
TRIM 21 Elimination of ICs via recruitment of the proteasomal machinery
a

No data are available.