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Biomedical subjects

M Kazatchkine

Publications and source records attributed to M Kazatchkine.

At least 73 records · Page 4Linked to original sources
PubMed1986

15-HETE "modulates" expression of C3b receptor (CR1) antigen on peripheral blood B-lymphocytes.

We have studied the effect of the lipoxygenase metabolite, 15-HETE, on the expression of the human C3b receptor (CR1) by a B-lymphocyte enriched population of human peripheral blood leukocytes. The number of CR1 antigenic sites expressed by B-lymphocytes isolated from HLA typed donors was determined by equilibrium binding studies using an 125 I-labelled mouse monoclonal anti CR1 antibody before and after 16 hrs incubation in RPMI alone or containing 10(-6)M, 10(-7)M or 10(-8)M final concentration of 15-HETE. In B44- subjects CR1 expression on B cells increased 63% after incubation in RPMI alone. This increase was inhibited in the presence of 10(-6)M and 10(-7)M 15-HETE (23% and 30% increase respectively). In contrast, B44+ individuals showed a smaller increase in CR1 numbers when incubated in RPMI alone. In the presence of 15-HETE CR1 antigenic sites continued to increase. When B44+ subjects were classified as A29+ or A29-, donors that were A29+ B44+ accounted for the augmentation observed while A29- B44+ individuals did not differ from individuals that were A29- B44-.

Antigens, Surface↗
PubMed1985

[Homozygotic C5 deficiency disclosed by purulent Neisseria meningitidis meningitis].

The complement system functions to protect the individual against infectious agents. Deficiencies of the late-acting complement proteins C5-C8 are associated with an increased susceptibility to Neisseria infection. This paper describes a deficiency in C5 in a Caucasoid family from the north of France that was revealed by the occurrence of a N. meningitidis meningitis in the homozygous C5-deficient propositus.

Adult↗
PubMed1985

Deficiency of the adhesive protein complex lymphocyte function antigen 1, complement receptor type 3, glycoprotein p150,95 in a girl with recurrent bacterial infections. Effects on phagocytic cells and lymphocyte functions.

A patient presenting delayed umbilical cord detachment, severe recurrent bacterial infections, and inability to form pus exhibited a profound defect in the expression of alpha- and beta-chains of the receptor for the C3bi fragment of C3 (CR3), lymphocyte function antigen 1 (LFA-1) molecule, and the p150,95 molecule found on neutrophils, monocytes, and lymphocyte membranes. This was shown by immunofluorescence studies using specific monoclonal antibodies, rosette formation with C3bi-coated erythrocytes, and immunoprecipitation for the LFA-1 complex. These membrane defects were responsible for abnormal phagocytic cell functions including adherence to nylon wool, cell movement, phagocytosis, and opsonized particle-induced oxidative response and for defective natural killer cell activity. In addition, lymphocyte function deficiencies previously unobserved in this disease were found. Cytolytic T lymphocyte activity was profoundly reduced; alpha- and gamma-interferon production were impaired. Finally, there was no antibody production to vaccinal antigens whereas the antibody responses to polysaccharides and to cytomegalovirus were found to be normal. The cytotoxic T cell deficiency could be expected from previous blocking experiments of this function with monoclonal antibodies to LFA-1 and is probably related to an extremely severe deficiency in LFA-1 expression in this patient. Anomalies in interferon and in antibody production suggest additional role(s) of the LFA-1 complex in monocyte/T lymphocyte/B lymphocyte cell interactions that have not yet been envisaged.

Antibodies, Monoclonal↗
PubMed1985

[The complement system in hepatopathies].

Low serum complement is often observed in cirrhosis of the liver. This is the result of two mechanisms: a failure to synthesise a certain number of components and regulatory proteins of complement, and an increased consumption due to activation of the complement system. This acquired deficit in complement contributes to the increased risk of infection in patients with cirrhosis.

Acute Disease↗
PubMed1984

[Alternative complement pathway].

The alternative complement pathway comprises three component proteins C3, B, D and three regulatory proteins P, H and I. These plasma proteins represent the major humoral defense mechanism against infection in a non-immune host. The following topics are reviewed: biochemistry of the alternative pathway proteins; molecular mechanisms of activation and regulation of the pathway; involvement of the alternative pathway in human diseases.

Antibody Formation↗
PubMed1984

[Monoclonal antibodies against surface antigens of lymphoblasts and blood cells or bone marrow recognize constituents of the human nephron].

By immunizing mice with bone marrow cells of a patient with acute lymphoblastic leukemia, monoclonal antibodies have been produced against differentiation antigens of hemopoietic cells. These antibodies also recognize cells in different parts of the normal human kidney. Two antibodies, ALB1 et ALB2, which recognize the common acute lymphoblastic leukemia antigen, (CALLA), label the podocytes and the epithelial cells of the proximal tubules of the kidney; ALB6, which recognizes the "p 24" antigen of lymphocytes, labels the distal tubules; ALB9, which recognizes lymphoblasts and granulocytes, labels the thick ascending loop of Henle and the collecting tubules; PM1, which recognizes immature granulocytic cells, labels the thick ascending loop of Henle.

Animals↗
PubMed1983

[Paroxysmal nocturnal hemoglobinuria. Increase in proteins of the alternative complement pathway].

Increased activity of the complement alternative pathway proteins C3, B and H was found in the sera of 16 patients with paroxysmal nocturnal haemoglobinuria (PNH). This increased activity might depend on protein hypersynthesis secondary to in vivo low-grade complement consumption by abnormal erythrocytes in PNH patients, despite the fact that serum levels of C3d were found to be normal. B and H activities were directly related; however, the B/H ratio was higher in patients whose sera had been taken early after an episode of haemoglobinuria. Activation of the alternative pathway, which is known to result in vitro lysis of PNH erythrocytes, only accounts for part of the events leading to chronic haemolysis and haemoglobinuria in vitro.

Adult↗
PubMed1983

The human C3b receptor.

The cellular receptor for the C3b fragment of the third component of complement is a 205,000 molecular weight glycoprotein expressed by erythrocytes, polymorphonuclear leukocytes, monocytes, B lymphocytes, a subset of T lymphocytes and glomerular podocytes. The receptor molecule is a potent inhibitor of complement activation by both the alternative and classical pathways. It serves as a cofactor in the proteolytic degradation of C3b bound to immune complexes. On neutrophils and monocytes, the receptor enhances immunoglobulin-dependent phagocytosis of opsonized particles and triggers internalization of soluble ligands bearing C3b. The number of C3b receptor molecules expressed on erythrocytes is genetically determined and was found to be low in patients with systemic lupus erythematosus: these abnormalities when associated with a low number of receptors in the kidney of patients with non-systemic lupus erythematosus nephritis may predispose to immune complex diseases.

Animals↗
PubMed1983

[The alternative complement pathway].

The alternative complement pathway comprises three component proteins C3, B, D and three regulatory proteins P, H and I. These plasma proteins represent the major humoral defense mechanism against infection in a non-immune host. The following topics are reviewed: biochemistry of the alternative pathway proteins; molecular mechanisms of activation and regulation of the pathway; involvement of the alternative pathway in human diseases.

Complement Activation↗
PubMed1979

[Alternative complement pathway (author's transl)].

The dual role of the alternative complement pathway in recognition of foreign substances by a non-immune host and in the intrinsic regulation of the complement sequence is now well recognized. Activation of this pathway occurs through escape from its regulatory mechanisms induced by the activating principle; its functional expression depends on the respective levels of the component proteins C3, factor B, factor D and properdin, and on the control proteins beta 1H and C3bINA. This article presents recently acquired knowlege on the molecular mechanisms of activation, regulation and behaviour under pathological conditions of the alternative complement pathway.

Complement Activation↗
PubMed1979

[The detection of soluble immune complexes (author's transl)].

The detection and characterization of soluble immune complexes is complicated by the broad spectrum of complexes occurring in human pathology. Thus, differences in immune complex size, specificity and ability to interact with immunologic effector systems such as complement or cells, suggest variable pathogenic potential. Therefore, a variety of techniques for detection should be available. The introduction of radioimmunoassays and the recently improved knowledge of immune complex biochemistry have lead to the description of a large number of detection procedures, which in turn has widened the catalogue of diseases associated with immune complexes. Among 50 procedures known today, this article selects some pertinent tests which are critically discussed with respect to their specificity, sensitivity and possible interest in clinical medicine.

Antigen-Antibody Complex↗
PubMed1976

Bleeding in renal failure: a possible cause.

Increased concentrations of factor VIII-related antigen (VIIIRA), factor VIII-procoagulant activity (VIIC), and decreased factor VII-von Willebrand activity (VIIIVWF) were found in the plasma of patients with chronic renal failure (CRF). This functional abnormality of the factor VII protein may partly explain the prolonged bleeding time commonly found in CRF. It was not improved by dialysis, but it was no longer found in patients with normally functioning grafted kidneys after the sixth month after transplantation. VIIIVWF levels remained decreased when compared with VIIIRA or VIIIC in transplanted patients undergoing acute reversible rejection soon after transplantation. Yet, not only VIIIC and VIIIRA but also VIIIVWF were greatly increased in patients with hyperacute irreversible rejection. Possibly a high VIIIVWF level in these patients is a thrombogenic factor.

Antigens↗
PubMed1976

[Reduction of Willebrand activity in patients with chronic kidney failure].

Decreased factor VIII von Willebrand activity in contrast with increased factor VIII procoagulant activity and increased concentrations of factor VIII related antigen, were found in the plasma of patients with chronic renal failure. This functional abnormality of the factor VIII protein is not improved by haemodialysis, but it is no longer found in patients with normally functioning grafted kidneys. It may at least partly explain the prolonged bleeding time commonly found in chronic renal failure.

Blood Coagulation Disorders↗
PubMed1976

[Recurrent polyneuropathy with a 19-year course, associated with a benign IgG monoclonal gammapathy].

A case of recurrent polyradiculoneuritis in a 54-year-old man is described. It is exceptional because of its lengthy development over a period of 19 years and by its association with a paraprotein of the IgE type without anyother anomal. Corticotherapy had a favourable effect on the clinical symptoms but did not affect the amount of monoclonal immunoglobulin in the serum. The nosological position of this neuropathy and the type of gammapathy are discussed. An immune mechanism seems likely, but no proof of a link between the neuropathy and the gammapathy could be found.

Bone Marrow↗
PubMed1976

[The role of thrombosis in renal allograft rejection (author's transl)].

Platelets and intravascular coagulation are involed in the pathogenesis of renal allotransplant rejection phenomena: fibrin deposition is a prominent feature of hyperacute rejection; arteriolar microthromboses when they are present, worsen the prognosis of an acute reversible rejection; the organisation of platelets and fibrin deposits on the intima may lead to the "endarteritis obilterans" of chronic bascular rejection. The interactions between endothelium, platelets, coagulation, fibrinolysis and cellular or humoral effectors of the immune respone were studied and special reference was made to their role in vascular rejection. The poor prognosis in vasuclar lesions justifies therapeutic trials with drugs inhibiting the early events of thrombogenesis.

Acute Disease↗