Complement C5
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Subject Areas on Research
- A simplified method for purification of human C5a from citrated plasma.
- Activation of the respiratory burst enzyme in human polymorphonuclear leukocytes by chemoattractants and other soluble stimuli. Evidence that the same oxidase is activated by different transductional mechanisms.
- Alterations of new methylated phospholipid synthesis in the plasma membranes of macrophages exposed to chemoattractants.
- Behçet's disease patients present high levels of deglycosylated anti-lipoteichoic acid IgG and high IL-8 production after lipoteichoic acid stimulation.
- C5a induction of human interleukin 1. Synergistic effect with endotoxin or interferon-gamma.
- C5a stimulates secretion of tumor necrosis factor from human mononuclear cells in vitro. Comparison with secretion of interleukin 1 beta and interleukin 1 alpha.
- Cellular serine proteinase induces chemotaxis by complement activation.
- Chemoattractant receptors on phagocytic cells.
- Complement in the pathophysiology of human disease.
- Component deficiencies. 5. The fifth component.
- Deficiency in C3b receptors on neutrophils of patients with chronic granulomatous disease and hyperimmunoglobulin-E recurrent infection (Job's) syndrome.
- Deficiency of the fifth component of complement in human subjects. Clinical, genetic and immunologic studies in a large kindred.
- Effect of pexelizumab in coronary artery bypass graft surgery with extended aortic cross-clamp time.
- Effect of pexelizumab on mortality in patients with acute myocardial infarction or undergoing coronary artery bypass surgery: a systematic overview.
- Effect of pexelizumab, an anti-C5 complement antibody, as adjunctive therapy to fibrinolysis in acute myocardial infarction: the COMPlement inhibition in myocardial infarction treated with thromboLYtics (COMPLY) trial.
- Effects of C5 complement inhibitor pexelizumab on outcome in high-risk coronary artery bypass grafting: combined results from the PRIMO-CABG I and II trials.
- Generation of a fibroblast chemotactic factor in serum by activation of complement.
- High predictive accuracy of an unbiased proteomic profile for sustained virologic response in chronic hepatitis C patients.
- Human C5a modulates monocyte Fc and C3 receptor expression.
- Inhaled asbestos activates a complement-dependent chemoattractant for macrophages.
- Inherited human complement C5 deficiency. Nonsense mutations in exons 1 (Gln1 to Stop) and 36 (Arg1458 to Stop) and compound heterozygosity in three African-American families.
- Leukocyte chemoattractant receptors.
- Multimeric C9 within C5b-9 is required for inner membrane damage to Escherichia coli J5 during complement killing.
- Natural antibody and complement mediate neutralization of influenza virus in the absence of prior immunity.
- New developments in immunopathology with special reference to complement and immune complexes.
- Novel delivery of oligonucleotides using a topical hydrogel tissue sealant in a murine partial nephrectomy model.
- Pathogenicity of Saccharomyces cerevisiae in complement factor five-deficient mice.
- Patients with bone marrow failure demonstrate decreased cutaneous reactivity to human C5a.
- Pexelizumab, an anti-C5 complement antibody, as adjunctive therapy to primary percutaneous coronary intervention in acute myocardial infarction: the COMplement inhibition in Myocardial infarction treated with Angioplasty (COMMA) trial.
- Potential pathogenicity of deglycosylated IgG cross reactive with streptokinase and fibronectin in the serum of patients with rheumatoid arthritis.
- Prognostic significance of blood markers of inflammation in patients with ST-segment elevation myocardial infarction undergoing primary angioplasty and effects of pexelizumab, a C5 inhibitor: a substudy of the COMMA trial.
- Role of complement activation in obliterative bronchiolitis post-lung transplantation.
- Role of complement receptors 1 and 2 (CD35 and CD21), C3, C4, and C5 in survival by mice of Staphylococcus aureus bacteremia.
- Studies of human C5a as a mediator of inflammation in normal human skin.
- Studies on the fibronectin receptors of human peripheral blood leukocytes. Morphologic and functional characterization.
- Studies on the mechanism of bacterial resistance to complement-mediated killing. I. Terminal complement components are deposited and released from Salmonella minnesota S218 without causing bacterial death.
- Studies on the mechanism of bacterial resistance to complement-mediated killing. II. C8 and C9 release C5b67 from the surface of Salmonella minnesota S218 because the terminal complex does not insert into the bacterial outer membrane.
- Studies on the mechanism of bacterial resistance to complement-mediated killing. VI. IgG increases the bactericidal efficiency of C5b-9 for E. coli 0111B4 by acting at a step before C5 cleavage.
- Substance P primes human neutrophil activation: a mechanism for neurological regulation of inflammation.
- Terminal complement components play a role in the expression of C5a.
- The complement system in host defense and inflammation.
- The mechanism by which microorganisms avoid complement attack.
- Use of C6-deficient rats to evaluate the mechanism of hyperacute rejection of discordant cardiac xenografts.