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Biomedical subjects

Y Naparstek

Publications and source records attributed to Y Naparstek.

At least 37 records · Page 2Linked to original sources
PubMed1995

Immunoglobulins from rats that are resistant to adjuvant arthritis suppress the disease in arthritis-susceptible rats.

The therapeutic effect of high doses of polyclonal immunoglobulins has been well established in various B cell-associated autoimmune diseases. In the present work we have examined the effect of low doses of immunoglobulins in adjuvant arthritis, a T cell-associated disease in the Lewis rat. Lewis rats were treated with purified rat immunoglobulins as well as their Fc and F(ab')2 fragments and their protective effect on adjuvant arthritis was evaluated. We found that early as well as late treatment with low doses of rat immunoglobulins induced refractoriness to disease induction. The effect was found to be carried out by the F(ab')2 part of the immunoglobulins and could be adsorbed by affinity purification on Mycobacterium tuberculosis. The protective antibodies were present in Fisher and BN rats that are resistant to adjuvant arthritis, but not in the arthritis susceptible Lewis and Wistar strains. We suggest that resistance to autoimmune arthritis is associated with the presence of protective immunoglobulins and that their effect is carried out through the antigen recognition part of the molecule.

Animals↗
PubMed1995

The urine of SLE patients contains antibodies that bind to the laminin component of the extracellular matrix.

Direct immunofluorescence of tissues derived from patients affected with SLE demonstrates antibodies bound to the extracellular matrix (ECM). In the present work we have tested whether such antibodies are found in the serum and urine of lupus patients and mice. We found that the urine of patients with active SLE and of MRL/lpr/lpr mice contains antibodies that bind ECM and that a major target for these antibodies is the 200 kDa light chain of laminin which is one of the matrix components. The level of the anti-ECM, anti-laminin antibodies correlates with disease activity.

Albuminuria↗
PubMed1995

A study of Israeli blood donors, asymptomatic carriers of hepatitis C virus, in relation to liver disease, cryoglobulinemia and transmission.

In order to study the asymptomatic hepatitis C virus (HCV)-positive blood donors in Israel we analyzed their sera for HCV-RNA using the polymerase chain reaction technique. We found that 0.44% of blood donors were anti-HCV positive. Of those who had repeatedly positive anti-HCV, 82% had evidence of HCV-RNA. One-third of them had elevated liver enzymes, but no detectable cryoglobulins were found in their sera. Although HCV-RNA was detected in the majority of the patients, we were unable to demonstrate vertical or horizontal transmission among the family members of our carrier population.

Adult↗
PubMed1995

Successful treatment of pure red cell aplasia in systemic lupus erythematosus with erythropoietin.

We describe a 32-year-old woman who developed severe anemia due to pure red cell aplasia in the course of systemic lupus erythematosus (SLE). After failure of therapy with high doses of glucocorticoids and immunoglobulins, and despite high levels of endogenous erythropoietin, she was treated with human recombinant erythropoietin with dramatic and sustained improvement. Based on this case and on the literature review of erythropoietin therapy in pure red cell aplasia, we suggest that erythropoietin should be used in SLE associated pure red cell aplasia before cytotoxic therapy.

Adult↗
PubMed1993

IgA deficiency associated with chronic hepatitis C virus infection. A cause or an effect?

OBJECTIVE: To evaluate the role of IgA in hepatitis C virus (HCV) infection. We have tested serum IgA levels in patients with antibodies to HCV. DESIGN: A retrospective study. PATIENTS: The IgA levels were tested in serum samples from 94 patients with antibodies to HCV examined during 1989-1990. RESULTS: Low IgA levels were found in 16/94 (17%) patients. In three of these 16 patients (3.2% of the original 94), no IgA was detected by radial immunodiffusion. In nine of 16 patients, previous pre-HCV infection serum samples with undetectable anti-HCV antibodies were available. In four of these nine patients, IgA deficiency was found in the preinfection serum, while in the remaining five patients, previous IgA levels were normal and the occurrence of anti-HCV was associated with the recent development of IgA deficiency. CONCLUSIONS: The results of this study indicate that IgA deficiency is a risk factor for HCV infection in some patients, whereas in others it might be caused by the viral disease.

Adult↗
PubMed1993

Colchicine induced remission in amyloid nephrotic syndrome.

An unusual case of reversible reactive amyloidosis (AA) is described. A patient in the course of lobar pneumonia developed acute transient nephrotic syndrome and renal failure. Renal and liver biopsy showed amyloidosis and positive immunohistochemistry stains for amyloid A protein. The nephrotic syndrome resolved completely following 6 months of colchicine treatment and the urine is protein free after 6 years of follow-up.

Aged↗
PubMed1993

The role of autoantibodies in autoimmune disease.

In autoimmune diseases, autoantibodies may be the actual pathogenetic agents of the disease, the secondary consequences of tissue damage, or the harmless footprints of an etiologic agent. Establishing a pathogenetic role for autoantibodies requires that they meet stringent criteria. It appears that the location of the presumptive target antigen most critically influences the pathogenetic potential of autoantibodies. Autoantibodies directed against cell surface targets, such as hormone receptors, are clearly pathogenetic; those directed against extracellular targets, such as circulating molecules or extracellular matrix, may or may not cause any damage. Those apparently directed against intracellular targets are usually not pathogenetic unless it can be clearly demonstrated (a) that the antigen is released from within the cell so that it can bind onto a cell surface receptor or other extracellular location, such as proteinase 3; (b) that the antigen moves to an aberrant site on the cell surface, such as, perhaps, the small ribonucleoprotein antigen Ro; or (c) that a cross-reactive molecule, the actual target, such as the membrane ribosomal P-like protein, is at an accessible location.

Antigens, Surface↗
PubMed1993

Pure red cell aplasia associated with systemic lupus erythematosus: remission after a single course of intravenous immunoglobulin.

Pure red cell aplasia is characterized by severe anemia, with reticulocytopenia and absence of precursor cells in the bone marrow. Many modes of treatment have been described, including the use of immunosuppressive agents. Recently repeated courses of high-dose intravenous immunoglobulins have been used successfully in patients with idiopathic pure red cell aplasia. We here describe a 22-year-old woman who developed pure red cell aplasia in the course of systemic lupus erythematosus. After failure of corticosteroid therapy the patient was treated with one course of high-dose intravenous immunoglobulins with complete remission. No further therapy was required.

Adult↗
PubMed1993

Low-dose heparin inhibits acute graft versus host disease in mice.

We have studied the effect of low-dose heparin on GVHD, marrow engraftment and graft-versus-leukemia (GVL) effects in an experimental murine model. Recipient (C57BL/6 x BALB/c) F1 mice were transplanted with C57BL/6 marrow and/or spleen cells and treated with daily sc injection of 5 micrograms heparin for 30 days. We have shown that heparin in low doses attenuates the severity of acute GVHD and reduces the mortality rate from 69 to 37.5% without abrogating the GVL effect induced by the allograft and without impairing marrow engraftment.

Acute Disease↗
PubMed1992

Embryonal germ-layer antigens: target for autoimmunity.

Histopathological analysis of some systemic autoimmune diseases and syndromes led us to the conclusion that the common feature of the organs involved might be their embryonal origin. We suggest that organs derived from the same germ layer express common germ-layer-specific antigens. Such antigens could serve as target antigens for the autoimmune response.

Autoantibodies↗
PubMed1992

Expression of heparanase by platelets and circulating cells of the immune system: possible involvement in diapedesis and extravasation.

Interaction of T and B lymphocytes, platelets, granulocytes, macrophages and mast cells with the subendothelial extracellular matrix (ECM) is associated with degradation of heparan sulfate (HS) by a specific endoglycosidase (heparanase) activity. The enzyme is released from intracellular compartments (i.e., lysosomes, specific granules) in response to various activation signals (i.e., thrombin, calcium ionophore, immune complexes, antigens, mitogens), suggesting its regulated involvement in inflammation and cellular immunity. In contrast, various tumor cells appear to express and secrete heparanase in a constitutive manner, in correlation with their metastatic potential. Heparanase enzymes produced by different cell types may exhibit different molecular properties and substrate cleavage specificities. The platelet enzyme appears also in a latent form. It can be activated by tumor cells and thereby facilitate their extravasation in the process of metastasis. Degradation of ECM-HS by all cell types was facilitated by a proteolytic activity residing in the ECM and/or expressed by the invading cells. This proteolytic activity produced a more accessible substrate for the heparanase enzymes. Heparanase-inhibiting, nonanticoagulant species of heparin markedly reduced the incidence of lung metastasis in experimental animals. These species of heparin also significantly impaired the traffic of T lymphocytes and suppressed cellular immune reactivity and experimental autoimmune diseases. Heparanase activity expressed by intact cells (i.e., platelets, mast cells, neutrophils, lymphoma cells) was found to release active HS-bound basic fibroblast growth factor from ECM and basement membranes. Heparanase may thus elicit an indirect neovascular response in processes such as wound repair, inflammation and tumor development. The significant anticancerous effect of heparanase-inhibiting molecules may therefore be attributed to their potential inhibition of both tumor invasion and angiogenesis. Both normal leukocytic cells and metastatic tumor cells can enter the bloodstream, travel to distant sites and extravasate to the parenchyma at these sites. We suggest that heparanase is utilized for this purpose by both types of cells. Other functions (i.e., enzyme activities, adhesive interactions, chemotactic and proliferative responses) of metastatic tumor cells seem to mimic the equivalent functions of leukocytes as they migrate across blood vessels to gain access to sites of inflammation.

Animals↗