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At least 415 records · Page 23Linked to original sources
PubMed1988

Production of C3 nephritic factor by cultured lymphocytes derived from a patient with partial lipodystrophy.

C3 nephritic factor (C3 NeF) has been found mainly in the sera of patients with membranoproliferative glomerulonephritis (MPGN) and partial lipodystrophy (PLD). We examined whether peripheral blood mononuclear cells (PBMC) from a patient with PLD could produce C3 NeF. We investigated the in vitro immunoglobulin synthesis of PBMC with mitogen. We further studied the C3bBb stabilizing activity and undertook agglutination assays of the IgG obtained from the culture supernatants. The patient IgG was able to agglutinate only EAC4b3bBb cells and none of the other intermediate cells. We this demonstrated that C3 NeF could be produced in vitro by PBMC derived from a patient with PLD.

Child↗
PubMedDate not supplied

Mechanisms of loss of human neutrophil chemotaxis following thermal injury.

The increased susceptibility to infection of patients with thermal injury is related to loss of host defense, which is reflected, in part, by the temporal loss of chemotactic function of leukocytic phagocytes. Our studies of patient neutrophils to define the mechanism of this phenomenon involved evaluation of both random and chemotactic migratory functions of patient neutrophils, measurement of receptors for chemotactic ligands, and measurement of receptors mediating substrate adherence of the cells. Measurements of migratory functions were made using the under-agarose technique and measurements of receptor expression were accomplished by flow cytometry using fluorescein-labeled ligand or receptor-specific antibody. We conclude that loss of chemotaxis in response to C5a/C5adesArg is the results of down-regulation of receptors for C5a and of reduced motility, and that loss of chemotaxis in response to the tripeptide FMLP is the result of reduced motility alone. Measurements of changes in the expression of "adherence" (iC3b) receptors revealed that up-regulation occurs early and can be sustained for weeks after injury. These results are taken to suggest that either hyper- or hypo-adherence could explain the loss of random migratory function observed for patient cells. Evidence of auto-oxidative alteration of cytoskeletal elements, to produce loss of random migratory function, also is reviewed. Considering the evidence for activation of the complement cascade after thermal injury C5a and C5adesArg are likely primary factors in effecting the down-regulation of C5a receptors, stimulation of secretion to mobilize iC3b receptors, and stimulation of respiration to auto-oxidize cell components. Such evidence of injury-mediated complement activation included data derived from application of a novel immunoassay for iC3b.

Burns↗
PubMed1987

Clinical applications of crossed immunoelectrophoresis to the study of complement activation.

The purpose of our study was to set up a reliable method for the measurement of complement activation by adapting the method of crossed immunoelectrophoresis. We utilised anti C3 antiserum and barbitone buffer, containing sufficient EDTA to prevent in vitro activation of complement. We studied 44 patients undergoing open heart surgery, with cardiopulmonary bypass (CPB) by the analysis of plasma samples taken during the operation, and also samples of plasma and dialysate effluent from patients with end stage renal failure undergoing continuous ambulatory peritoneal dialysis (CAPD). Measurements were also carried out on stored blood, aged serum and serum treated with varying doses of lipopolysaccharide (LPS). Complement activation occurs in 95% of patients during CPB with levels ranging from less than 4.5% to 11.3% of total C3, but there was no detectable activation in any pre-bypass sample. Negligible complement activation occurs in the plasma of CAPD patients, but the dialysate effluent gave results from undetectable levels to 31.7%, in the absence of clinical peritonitis. Variable in vitro complement activation occurs in aged serum, but it was not detectable in stored blood. Serum treated with LPS showed levels of activation directly proportional to the dose of LPS and measurable at a level of 0.1 microgram/ml of serum. The method had a coefficient of variation of 4.5%, and provides a reliable way of measuring complement activation in clinical situations such as cardiopulmonary bypass and peritoneal dialysis.

Cardiopulmonary Bypass↗
PubMed1987

Establishment and characterization of a human myeloid cell line from Philadelphia chromosome-negative myeloblastic leukemia arising in a patient with myelodysplastic syndrome.

A new hematopoietic cell line derived from a patient with Philadelphia chromosome (Ph1)-negative myeloblastic leukemia arising from a form of myelodysplastic syndrome (MDS) is described. This cell line, designated TMM, consists of immature cells with the morphological characteristics of young myeloblasts and grows in suspension culture with a doubling time of about 30 hours. By cytochemical analysis the cultured cells were positive for acid phosphatase. They were free of the Epstein-Barr virus-associated nuclear antigen as well as terminal deoxynucleotidyl transferase. Further phenotypic analysis revealed the expression of the myelomonocytic-specific antigen Leu-M1 and receptors for the Fc portion of IgG. Partial differentiation of these cells could be induced by dimethyl sulfoxide, tetradecanoyl phorbol acetate, or hypoxanthine and resulted in cells of the myeloid series expressing lysozyme and receptors for the C3b complement protein. The karyotype was 46,XY, lacked the Ph1 chromosome, and displayed no abnormalities at the light microscopic level. No rearrangement of the bcr-c-abl gene complex was found. This cell line should be useful for studying an important type of the heterogeneous population constituting Ph1-negative myeloblastic leukemia, arising in this instance from MDS, as well as for studying differentiation and proliferation of human pluripotent stem cells.

Antigens, Neoplasm↗
PubMed1986

Relationship between the component and regulatory proteins of the classical pathway C3 convertase.

A relationship was found between the sums of the component proteins of the classical pathway C3 convertase (C2 and C4) and their regulators (C4bp and 1) in 184 normal controls. The relationship was maintained in most patients with low levels of individual components resulting from congenital deficiency and urinary losses, as well as in most cord sera. On the other hand, classical pathway activation in membranoproliferative glomerulonephritis type I, systemic lupus erythematosus, hereditary angioneurotic edema, and bacteremia resulted in loss of this relationship. Patients with alternative pathway-mediated complement activation (membranoproliferative glomerulonephritis type II) had a normal relationship between the classical component and regulatory proteins. In situations in which classical pathway activation is suspected, simultaneous examination of C4, C2, C4bp, and I may be helpful.

Angioedema↗
PubMed1979

A comparison of immunologic profiles and their influence on bacteremia in surgical patients with a high risk of infection.

Prospective sequential studies of the antibacterial function of neutrophils, lymphocyte responsiveness, opsonic capacity of serum and serum levels of C3(B), properdin, factor B, IgG, and albumin were made in 32 patients with severe burn injury (greater than or equal to 45%), 21 patients with severe multisystem traumatic injury, 20 high-risk, infected patients, and 22 renal transplant patients. Fifty-five episodes of bacteremia occurred in 37 of the 95 patients. Abnormal neutrophil function was clearly associated as a predisposing factor to these episodes, whereas there was no association between bacteremia and low serum levels of C3, IgG, factor B, or properdin. C3, factor B, and IgG usually rose following bacteremia as acute phase proteins, but there was evidence of a consumptive opsoninopathy in 11% of episodes. Defective opsonization was associated with a high risk of bacteremia only when there was a coexisting abnormality of neutrophil function (88% of such patients became bacteremic). None of 27 nonburned patients tested with delayed hypersensitivity antigens responded normally, and there was regularly depression of lymphocyte responsiveness to phytohemagglutinin-A and concanavalin-A in a whole blood assay related to serum immunosuppressive factors, but poor responsiveness was not associated with bacteremia.

Adolescent↗
PubMed1985

A synthetic nonapeptide corresponding to the NH2-terminal sequence of C3d-K causes leukocytosis in rabbits.

Numerous biologically active fragments have been described that are derived from the C3 molecule. Recently, a polypeptide (Mr 41,000) generated from the alpha chain of human iC3b by limited proteolysis with plasma kallikrein was shown to exhibit several biological functions. This C3-derived cleavage product, C3d-K, suppresses mitogen- and antigen-induced proliferation of human T-lymphocytes and induces leukocytosis in rabbits. We have identified and synthesized a portion of C3d-K that is associated with the leukocytosis phenomenon. A nonapeptide corresponding to the amino-terminal nine residues of C3d-K was synthesized using conventional Merrifield solid-phase peptide chemistry; the structure of this peptide is Thr-Leu-Asp-Pro-Glu-Arg-Leu-Gly-Arg (TLDPERLGR). At a final concentration of 4 X 10(-6) M, both the nonapeptide and the des-Arg octapeptide (TLDPERLG) were capable of inducing leukocytosis in rabbits. Additionally, both peptides enhance vascular permeability when injected in guinea pig skin. These activities are similar to those previously attributed to a C3 fragment identified as C3e by Ghebrehiwet and Müller-Eberhard (Ghebrehiwet, B., and Müller-Eberhard, H.J. (1979) J. Immunol. 123, 616-621). We conclude that the nonapeptide TLDPERLGR represents the active center of the C3-derived leukocytosis factors C3e and C3d-K. This active synthetic analogue of C3d-K should prove valuable in elucidating the mechanism of action for complement-dependent leukocyte mobilization in vivo.

Amino Acid Sequence↗
PubMed1985

Ontogeny of the third component of complement of Japanese quails.

Ontogeny of quail complement was examined in terms of serum C3 level, cytolytic activity of total complement, functional activity of C3 via the classical pathway (CCP) and an alternative route (ACP), and the distribution of C3-bearing cells. In serum, C3 was detected from 7-day-old embryos by rocket immunoelectrophoresis. Thereafter, its concentration increased rapidly and reached the adult level at 4-5 weeks of age. Total activities of serum complement via CCP and ACP, both of which were assayed by cell lysis, were detected first in 10-day-old embryos, and increased sharply after hatching, reaching the maximum level at 5 weeks of age. Deposition of C3 on the cell surface via CCP and ACP was also clearly demonstrated from 10-day-old embryos by haemagglutination and immunofluorescence techniques, respectively. By an immunofluorescence technique using anti-quail C3 monospecific serum, cells belonging to the reticuloendothelial system were indicated to serve major sites for the synthesis of C3 during ontogenesis.

Aging↗
PubMedDate not supplied

The biological role of the complement system and the clinical importance of complement measurements.

Properties of serum proteins belonging to the complement system, two pathways of the complement activation (classical and alternative pathway) as well as the physiological role of the complement system are discussed. Complement has essential importance in some physiological processes: In the induction of the humoral immune response, in the elimination of immune complexes and in the protection against bacterial and viral infections. After a short discussion of the genetics of the complement system, the principle and possibilities of clinical applications of the complement measurements are described. Finally, different approaches to the therapeutic manipulation of the complement system are discussed.

Angioedema↗