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. 2015 Mar 2;6:83. doi: 10.3389/fimmu.2015.00083

Table 3.

Modulation of TLR function by Siglecs adapted from Ref. (95, 155, 156).

Molecules TLR ligands used Cell type Observed phenotype
CD22 TLR3, 4, 7, and 9 B Enhanced proliferation of CD22 KO B cells
Siglec-G TLR3, 4, 7, and 9 B Enhanced proliferation of Siglec-G KO B cells
HMGB1 DC Enhanced TNF-α production in Siglec-G KO DCs
Siglec-E TLR4 Mac Reduced IL-12 production by cross-linking with Abs
Siglec-H TLR9 pDC Reduced IFN-α production by cross-linking with Abs
Siglec-5 TLR2, 3, 4, and 9 Mac Reduced TNF-α and enhanced IL-10 production by over-expression
Siglec-9 TLR2, 3, 4, and 9 Mac Reduced TNF-α and enhanced IL-10 production by over-expression
Siglec-11 TLR4 Mac Reduced IL-1β transcript by cross-linking with Abs
Siglec-14 TLR4 Mac Augmented TNF-α production by over-expression
CD33/Siglec-3 TLR4/CD14 imDCs Reduced the phosphorylation of NF-κB
Siglec-9 TLR2 Mac Siglecs exhibit lectin-dependent changes in cellular localization, which may be partly linked to its control mechanism that increases the production of IL-10