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A CD14-independent LPS receptor cluster
TLDR
Evidence is presented that implicates heat shock proteins 70 and 90, chemokine receptor 4 and growth differentiation factor 5 as the main mediators of activation by bacterial lipopolysaccharide. Expand
Population Pharmacokinetics and Pharmacodynamics of the Anti-CD11a Antibody hu1124 in Human Subjects with Psoriasis
TLDR
The pharmacokinetics of hu1124, a human anti-CD11a antibody, were investigated in human subjects with psoriasis and one of the receptor-mediated pharmacokinetic/pharmacodynamic models which was developed describes the dynamic interaction of hU1124 binding to CD11a, resulting in the removal of hi1124 from the circulation and reduction of cell surface CD 11a. Expand
Effects of administration of a single dose of a humanized monoclonal antibody to CD11a on the immunobiology and clinical activity of psoriasis.
TLDR
Targeting CD11a may improve psoriasis by inhibiting T-cell activation, T-cells emigration into the skin, and cytotoxic T- cell function. Expand
Psoriasis as a model for T-cell-mediated disease: immunobiologic and clinical effects of treatment with multiple doses of efalizumab, an anti-CD11a antibody.
TLDR
At doses of 0.3 mg/kg or more per week, intravenous efalizumab produced significant clinical and histologic improvement in psoriasis, which correlated with sustained serum efalIZumab levels and T-cell CD11a saturation and down-modulation. Expand
Targeted Deletion of the Lipopolysaccharide (LPS)-binding Protein Gene Leads to Profound Suppression of LPS Responses Ex Vivo, whereas In Vivo Responses Remain Intact
TLDR
Data suggest the presence of an LBP-independent mechanism for responding to LPS, and these LBP knockout mice may provide a tool for discovering the nature of the presumed second mechanism for transferring LPS to responsive cells. Expand
Pharmacokinetic–Pharmacodynamic–Efficacy Analysis of Efalizumab in Patients with Moderate to Severe Psoriasis
TLDR
Simulations using the final model suggested that efalizumab administered less frequently could possibly be more convenient with similar efficacy, and the PK/PD/E data in psoriasis patients reasonably well. Expand
Sequence elements required for activity of a murine major histocompatibility complex class II promoter bind common and cell-type-specific nuclear factors.
TLDR
Analysis of sequence elements and corresponding DNA-binding factors required for transient expression of the A alpha d promoter fused to the bacterial chloramphenicol acetyltransferase reporter gene in a variety of cultured cell lines showed that the three most predominant factors present in extracts from WEHI-3, A20, or L cells are actually a family of factors that bind to a fourth sequence element that is homologous to the cyclic AMP-responsive enhancer element. Expand
Fluorescence recovery after photobleaching reveals that LPS rapidly transfers from CD14 to hsp70 and hsp90 on the cell membrane.
TLDR
Hsps are implicated as mediators of the innate activation by bacteria after the diffusion coefficient of CD14 remains unaffected after LPS ligation and that the diffusion coefficients of FITC-LPS and FITc-LTA bound to cells differ from that ofCD14. Expand
Phospholipids Inhibit Lipopolysaccharide (LPS)-Induced Cell Activation: A Role for LPS-Binding Protein1
TLDR
It is shown that LBP is a target for the inhibitory function of phospholipids, and experiments investigating the LBP-mediated intercalation of LPS andospholipid liposomes mimicking the macrophage membrane could show that preincubation of soluble LBP with phospholIPids leads to a significant reduction of LPD. Expand
Biochemical Characterization of Recombinant Fusions of Lipopolysaccharide Binding Protein and Bactericidal/Permeability-increasing Protein
TLDR
How closely related proteins such as BPI and LBP can have opposing effects on the body's response to LPS is defined by comparing the functional activities and pharmacokinetics of these fusions, the individual N-terminal domains, and the parent proteins. Expand
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