PMID: 9665271, 2471708 LBP clearly binds LPS (and LPS substructures, such as lipid IVa) through the recognition of lipid A.

PMID: 9665271 high concentrations of Taxol induced minimal interferoninducible protein-10 (IP-10) expression in the CD14-/- mice, even though induction of TNF-a and interleukin-1b expression occurred.

PMID: 9665271 high concentrations of Taxol induced minimal interferoninducible protein-10 (IP-10) expression in the CD14-/- mice, even though induction of TNF-a and interleukin-1b expression occurred.

PMID: 9665271 In the case of LPS activation of IL-6 expression, CD14-independent induction of IL-6 expression does not appear to involve monocytic cells, whereas maximal expression of IL-6 in vivo still requires both macrophages and CD14-dependent signaling.

PMID: 9665271 LPS-inducible IP-10 expression in vivo appears to be the most dependent on CD14-dependent signaling.

PMID: 9665271 TNF-alpha and IL-1b expression can be induced by both CD14-dependent and -independent pathways.

PMID: 9665271 TNF-alpha and IL-1b expression can be induced by both CD14-dependent and -independent pathways.

PMID: 9665271 High levels of SR-A expression by activated macrophages may favor the uptake of LPS by this receptor, thus leading to a net reduction in free LPS that would be available to bind CD14.

PMID: 9665271 Three cloned molecules expressed on the surface of monocytes and macrophages are known to bind the lipid A moiety of LPS. These include CD14, the macrophage scavenger receptor (SR), and the beta2 leukocyte integrins (CD11a/CD18, CD11b/ CD18, and CD11c/CD18; this family of receptors herein will be referred to as CD11/18).

PMID:9665271 In the case of LPS activation of IL-6 expression, CD14-independent induction of IL-6 expression does not appear to involve monocytic cells, whereas maximal expression of IL-6 in vivo still requires both macrophages and CD14-dependent signaling.

PMID: 9665271 TNF-alpha and IL-1b expression can be induced by both CD14-dependent and -independent pathways.

PMID: 99652871, 7505800, 1698311, 1607653, 8666811 LPS binds stoichiometrically to CD14. LBP moves LPS onto CD14.

PMID: 9665271 The SR-A is expressed by activated macrophages and able to bind a broad range of polyanionic ligands, including LPS, modified lipoproteins, and lipoteichoic acid of Gram-positive bacteria.

PMID: 9665271 The SR-A is expressed by activated macrophages and able to bind a broad range of polyanionic ligands, including LPS, modified lipoproteins, and lipoteichoic acid of Gram-positive bacteria.

PMID: 9665271 LBP mediates the transfer of LPS and/or the inhibitors onto CD14. PMID: 9665271 This model reflects our findings that the LPS-like molecules RSLA and lipid IVa function as antagonists in human macrophages

PMID: 9665271 LBP mediates the transfer of LPS and/or the inhibitors onto CD14. PMID: 9665271 This model reflects our findings that the LPS-like molecules RSLA and lipid IVa function as antagonists in human macrophages

PMID: 9665271 CD14 then transfers the ligand to a signal transducer (shown here as a transmembrane molecule). LPS inhibitors prevent the transfer of LPS from CD14 to its associated signal transducer.

PMID: 9665271 the engagement of LPS by CD14 that occurs in tissues does not always occur as an LBP-mediated event.

PMID: 9665271 LPS interacts with high concentrations of locally secreted sCD14.

PMID: 9665271 high concentrations of Taxol induced minimal interferoninducible protein-10 (IP-10) expression in the CD14-/- mice, even though induction of TNF-a and interleukin-1b expression occurred.

PMID: 9665271 residual TNF-a production in response to LPS challenge was observed in the CD14-/- mice.