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S J Sierakowski

Publications and source records attributed to S J Sierakowski.

15 recordsLinked to original sources
PubMed1993

Lithium in vitro enhances interleukin-2 production by T cells from patients with systemic lupus erythematosus.

Cellular immunity is impaired in patients with systemic lupus erythematosus (SLE). A decreased production of interleukin-2 by T cells isolated from blood of patients with SLE was found. The decrease correlated with severity of the disease. It was shown that incubation in vitro of T cells with 5 mM of lithium chloride augmented interleukin-2 production. The increase in cultures of T cells from patients with SLE was higher that than in healthy individuals. It is believed that lithium increases the cytosol inositol triphosphate level and subsequently augmented impaired intracellular signal transduction in the T cells from patients with SLE.

Adult↗
PubMed1990

Studies on immunomodulatory properties of isoniazid. IV. Effect of isoniazid on T lymphocyte activation by phorbol ester tumor promoter.

Human peripheral blood T cells or continuous T cell lines were treated with phorbol myristate (PMA), a direct protein kinase C activator. The effect of isoniazid on PMA-treated cells was investigated. It was found that low doses of isoniazid augmented proliferation of T cells treated with PMA or stimulated with PMA and phytohemagglutinin. Similar results were shown in the Jurkat cell line. There was no influence of isoniazid upon proliferation of PMA-treated HT-2 cells, interleukin 2-dependent cell line. The obtained results suggest that, at least one target mechanism of isoniazid is located in T cell activation pathway after protein kinase C activation.

Adjuvants, Immunologic↗
PubMed1990

Studies on immunomodulatory properties of isoniazid. I. Effect of isoniazid on mitogen- and anti-CD3 antibody-induced proliferation of human peripheral blood mononuclear cells and T cells.

Isoniazid, a tuberculostatic agent, induced in some patients lupus-like syndrome. Pathomechanism of this autoimmune phenomenon is unknown, and it is suggested that is associated with disturbances in immunoregulatory processes. Human peripheral blood mononuclear cells or T cells were isolated from healthy donors and were stimulated with phytohemagglutinin or antibody against CD3 cell receptor antigen. Proliferation, measured as thymidine uptake, was determined in in vitro cultures of the cells. Isoniazid added to cell cultures decreased proliferation at higher doses, and produced a slight increase in proliferation in concentration 10(-5)-10(-6) M. Isoniazid alone has no mitogenic activity. The viability of the cells, determined as the Trypan blue exclusion test, was decreased only at the presence of the highest used dose of isoniazid (10(-2) M), thus the results were not influenced by the toxic effects of the drug.

Adult↗
PubMed1990

Studies on immunomodulatory properties of isoniazid. II. Effect of isoniazid on interleukin 2 production and interleukin 2-receptor expression.

The effect of isoniazid on interleukin 2 production and interleukin 2-receptor expression by phytohemagglutinin-stimulated human T cells was investigated. High concentrations of the drug decreased interleukin 2 production while low doses (10(-5)-10(-6) M) produced a slight increase in interleukin 2 production. Isoniazid did not affect the expression of interleukin 2-receptors on the surface of T cells, except a slight decrease in cells exposed to high levels of the drug.

Cell Division↗
PubMed1990

Studies on immunomodulatory properties of isoniazid. III. Effect of isoniazid on proliferation of interleukin-dependent and interleukin-independent cell line.

The effect of various concentrations of isoniazid on proliferation of the interleukin 2-dependent cell line, HT-2 and continuous T cell line Jurkat was studied. It was found that high doses of isoniazid increased proliferation of the HT-2 cells in presence of suboptimal doses of interleukin 2. Low doses had no effect on proliferation. The unstimulated Jurkat cells increased proliferation in presence of low doses of isoniazid while phytohemagglutinin-stimulated cells responded to high doses of the drug only. It is hypothesized that biphasic effect of isoniazid is caused by cumulation of direct and indirect effects of T cell activation as well as toxic influence on the cells.

Animals↗
PubMed1989

[Metabolism of the connective tissue in generalized scleroderma].

Scleroderma, a connective tissue disorder is characterized by vascular and interstitial reaction with deposition of matrix components. Abnormalities in collagen and glycosaminoglycan structure and metabolism, and regulatory processes of their biosynthesis in scleroderma are reviewed.

Collagen↗
PubMed1988

Effect of copper on activation of human T cells.

Immunomodulatory properties of copper were investigated. Human T cells, isolated from blood of healthy donors, were stimulated with phytohemagglutinin and cultured in vitro. It was found that copper sulphate depressed T cell proliferation when added in concentration of 10(-3) M. A slight increase in the T cell proliferation was shown in presence of 10(-5) M of copper ion while 10(-7)-10(-9) M had no effect on proliferation. Production of interleukin 2 by human T cells was depressed by all investigated doses of copper. The obtained results suggest the direct toxicity of copper on T cell activation.

Cells, Cultured↗
PubMed1988

Thrombotic thrombocytopenic purpura. A review.

Thrombotic thrombocytopenic purpura (Moschcowitz's disease) is an uncommon, life-threatening disorder of unknown cause. It consists of fluctuating symptoms including: haemolytic anemia, fever, thrombocytopenia, neurological and mental disturbances, and renal dysfunctions. The high mortality of this disease necessitates rapid diagnosis and immediate therapy. The clinical manifestations and diagnostic criteria are reviewed. A variety of theories have been proposed to explain its clinical and pathological manifestations, but the pathophysiology remains poorly understood. The present knowledge of the pathophysiology is discussed in detail. Failure to define the pathophysiology is a reason why there are no widely accepted therapeutic recommendations. The modes of therapy of the disease in relation to current understanding of its nature are discussed. The effect of exchange transfusions, plasma infusions, plasmapheresis and plasma exchange, corticosteroid therapy, immunosuppressive drugs, antiplatelet therapy and splenectomy on clinical course are reviewed.

Adolescent↗
PubMedDate not supplied

T cell subsets in patients with systemic lupus erythematosus.

T cell subsets were determined in blood of 16 patients with systemic lupus erythematosus (SLE), and 16 healthy individuals. SLE patients showed marked decrease in relative level of suppressor/cytotoxic T cells, slight decrease in helper/inducer T cells, and an increased helper/suppressor T cell ratio. The diminished level of suppressor/cytotoxic T cells was correlated with the clinical severity of disease. Cytofluorographic analysis of T cell subsets obtained from SLE patients did not show significant differences in homogeneity of the cell subpopulations as compared to healthy controls.

Cell Separation↗