. 2013 Jun;93(6):847–863. doi: 10.1189/jlb.1012501

Table 1. Overview of TLRs, Agonists, and Use in Cancer Therapeutics.

TLR	Cellular localization	Adaptor molecule	Ligand/agonist	Source of ligand	Clinical
TLR1-TLR2	Surface	MyD88	Triacylated lipoproteins, lipoteichoic acid, peptidoglycans	Bacteria	BCG^a
			Zymosan	Fungi	–
			Pam₃CSK₄	Synthetic	–
TLR2-TLR6	Surface	MyD88	Diacylated lipopeptides	Bacteria	BCG^a
			HSPs, HMGB1, uric acid, fibronectin, ECM proteins	Endogenous	–
			Pam₃CSK₄	Synthetic	–
TLR3	Endosome	TRIF	dsRNA	Virus	–
TLR3	Endosome	TRIF	Poly I:C	Synthetic	Poly A:U
TLR4	Surface (or endosome)	MyD88 or TRIF	LPS, lipoteichoic acid	Bacteria	BCG^a
			β-defensin 2, fibronectin EDA, HMGB1, snapin, tenascin C	Endogenous
				Synthetic	MPL^a
TLR5	Surface	MyD88	Flagellin	Bacteria	–
TLR7-TLR8	Endosome	MyD88	ssRNA	Virus	–
TLR7-TLR8	Endosome	MyD88	CpG-A, Poly G10, Poly G3	Synthetic	Imiquimod (Aldara)^a 852A (Phase II)
TLR9	Endosome	MyD88	Unmethylated CpG DNA	Bacteria and virus	–
				Bacteria	BCG^a
				Synthetic	EMD 120108 (Phase I)
				Synthetic	IMO-2055 (Phase II)
TLR10	Surface	MyD88	Unknown natural ligand	Synthetic	–
TLR10	Surface	MyD88	Pam₃CSK₄, PamCysPamSK₄	Synthetic
TLR11^b	–	–	Toxoplasma gondii profilin	Protozoa	–
TLR12^b	–	–	Unknown	–	–
TLR13^b	Endosome	MyD88	VSV	Virus	–

TLRs are characterized by their cellular localization, adaptor proteins, and the PAMPs and DAMPs that they recognize. Agonists come from a variety of sources—natural and synthetic. Several TLR agonists are approved for clinical use, whereas others are being tested in clinical trials for their potential as anticancer therapies.

FDA-approved treatment for cancer;

expression detected in mouse cells but not human cells.