Tlr4- Cluster of Differentiation 284

 association of an additional component, MD-2 which
Toll-like receptor 4 (TLR4) often designated as CD284together can initiate two major intracellular signaling
(cluster of differentiation 284) is a class Ipathways, MyD88-dependent and TRIF-dependent
transmembrane receptor belonging to the large(MyD88-independent). The MyD88-dependent pathway
homologous family of Toll like receptors. TLR4requires the recruitment of TIRAP and MyD88 via
expressed on the surface of immune system cells, ishomophilic TIR-TIR interactions and activates nuclear
activated by exposure to lipopolysaccharides derivedfactor (NF)-?B, activator protein-1 (AP-1) and interferon
from the outer membrane of Gram negative bacteriaregulatory factor 5 (IRF5), which induce inflammatory
and thus forms part of the innate immune response incytokine expression such as IL-6, IL-12, and TNF?. The
mammals. (1) TLR4 was initially cloned as the humanTRIF-dependent pathway requires the recruitment of
homolog of Drosophila Toll (dToll) and thus was firstTRAM and TRIF and activates IRF3, in addition to
named hToll. Like all other members of the TLR family,NF-?B and AP-1, which induce type I interferon (IFN)
TLR4 is composed of an extracellular domainexpression. TLR4 can also activate various other
containing multiple leucine-rich repeats (LRRs), asignaling molecules, including phosphatidylinositol-3
transmembrane region, and a cytoplasmic tailkinase (PI-3K) and MAP3Ks such as MEKK3, TPL2,
containing the conserved TIR domain. TLR4 maps toand ASK1. (5,6) The TLR4 complex also recognizes a
chromosome 9q32-33. It shows a high degree offew other bacterial PAMPs including LTA. Further, the
similarity to dToll over the entire aminoacid sequence.TLR4 complex recognizes viruses including respiratory
The TLR4 sequence encodes an 839 aminoacidsyncytial virus (RSV), hepatitis C virus (HCV), and
protein with 22 N-terminal LRR regions and amouse mammary tumor virus (MMTV). The TLR4
calculated molecular weight of 90 kDa. TLR4 is mostcomplex can also recognize endogenous ligands, for
closely related to TLR1 and TLR6 each with 25%example, heat shock proteins, fibrinogen, fibronectin,
overall aa sequence identity. Several transcript variantssurfactant protein A (SP-A), and ?-defensins. TLR4
of this gene have been found, but the protein codingalso forms heterodimers both with TLR5, which
potential of most of them is uncertain.presumably enhances its activity, and also with TLR1,
 which inhibits its activity. (7, 8)
In vivo, TLR4 mRNA is expressed as a single 
transcript, and found at highest levels in spleen andMutations in TLR4 gene have been associated with
PBLs. (2, 3) Of the PBL populations, TLR4 isdifferences in LPS responsiveness.
expressed by B cells, DCs, monocytes, macrophages,A recently discovered Asp299Gly TLR4
granulocytes, and T cells. Other reports suggest thatpolymorphism has been identified that confer
TLR4 is only expressed in myelomonocytic cells and isdifferences in the inflammatory response elicited by
highest in mononuclear cells. In vitro, TLR4 mRNA andbacterial lipopolysaccharide and is associated with a
protein expression is upregulated in THP-1 cells upondecreased risk of atherosclerosis. (9)
PMA-induced differentiation. TLR4 is moderately 
upregulated by autocrine IFN-?, IL-1?. TLR4 mRNAReference:
expression in THP-1 cells is unaffected by exposure to1. Ricardo et al. PLoS ONE. 2007; 2(8): e788.
both Gram-positive and Gram-negative bacteria. Ex2. Medzhitov, R. et al. (1997) Nature 388:394.
vivo, granulocyte, and especially monocyte, TLR43. Rock, F.L. et al. (1998) Proc. Natl. Acad. Sci. USA
expression is upregulated upon exposure to95:588.
Gram-negative bacteria. (4)4. Zarember, K.A. & P.J. Godowski (2002) J. Immunol.
 168:554.
TLR4 is critical for host defense against5. Myeong Sup Lee Vol. 76: 447-480 Annual Review
gram-negative bacteria in both mice and humans. Uponof Biochemistry
recognition of its ligand LPS, TLR4 undergoes6. Yong-Chen Lu doi:10.1016/j.cyto.2008.01.006  Article
dimerization, and recent studies suggest that thisin press
causes concerted conformational changes in the7. Spitzer, J.H. et al. (2002) Eur. J. Immunol. 32:1182.
receptor leading to self association of the cytoplasmic8. Mizel, S.B. et al. (2003) J. Immunol. 170:6217.
Toll/Interleukin 1 receptor (TIR) signalling domain. Ligand9. N Engl J Med 2002; 347:1978-1980, Dec 12, 2002.
recognition by TLR4 requires the extracellular