Biomedical subjects

K E Wiktorowicz

Publications and source records attributed to K E Wiktorowicz.

7 recordsLinked to original sources

PubMed1996

The lymphocyte phenotype in patients with primary fibromyalgia.

The aim of this study was to examine the lymphocyte phenotype in fibromyalgia (FB) patients. Nineteen patients [18 females, 1 male] who met the ACR classification criteria for FB were recruited into the study. The fluorescence of leukocytes was measured using Ortho Cytotron Absolute flow cytometer. Ortho-mune monoclonal antibodies [OK-Combo-Tests] were used for determination of the following antigens: CD3/CD19, CD3/HLA-DR, CD4/CD8, CD45RA/CD4. Serum IgE was established with ELISA [Merck, Germany]. There were no differences in percentage of CD3, CD19, CD4, CD8, CD3/HLA-DR and CD4/CD45RA cells as compared to healthy controls. We found a negative correlation between CD4 and CD8, CD3DR and IgE, CD8 and IgE concentration. The positive correlation between CD3 and CD3DR, CD3DR and CD8 was observed. The inhibitory effect of CD8+ cells subpopulation on B-cells and thereby on IgE production in patients afflicting for allergy has been already observed. Moreover, the symptoms to allergy has been found in about 50% of our patients. Taken together the data thus far obtained present a coexistence of symptoms of allergy and FB.

Adult↗

PubMed1994

Lymphocyte phenotype studies of rheumatoid arthritis patients treated with methotrexate.

Seventy nine patients with rheumatoid arthritis (RA) were monitored for 12 months. Forty eight individuals were treated weekly with a low dose of methotrexate (MTX), and 31 received nonsteroid antiinflammatory drugs (NSAID) only. The mean total dose of MTX was 413 mg with a range from 250 to 735 mg. The phenotype of lymphocytes was analyzed using double immunofluorescence and a panel of monoclonal antibodies. The clinical status of 33 MTX-treated patients improved, in 9 neither clinical nor laboratory improvement was noticed. Six patients were withdrawn from the study because of adverse reactions. We observed no changes in the percentage of CD3, CD4, CD8 and CD25 positive lymphocytes in both MTX and NSAID-treated groups. However, the percentage of CD19 positive cells significantly decreased during 12 month observation (15.1 +/- 6.5% v.s. 10.2 +/- 5.0, p < 0.01) in MTX-treated subjects. Moreover, this percentage increased (9.4 +/- 6.7% v.s. 17.1 +/- 1.1%, p < 0.01) in NSAID-treated patients.

Adult↗

PubMed1994

Contrasting effect of oral and intravenous cyclophosphamide treatment on phenotypes of human peripheral blood lymphocytes.

Twenty three rheumatoid arthritis (RA) patients treated with cyclophosphamide (CTX) were observed for 6 months. Eight patients received CTX in a single intravenous dose (group I) and 15 orally in a single daily dose (group II). The surface antigens of lymphocytes, isolated from peripheral blood, were determined using immunofluorescence method. The clinical improvement was observed both in group I and in group II of patients. However, in patients receiving CTX intravenously amelioration of the disease appeared quicker. The percentage of CD3+ and CD8+ T cells remained unchanged. In group I we observed decrease in the number of CD4+ T cells (60.1 +/- 11.5% and 43.8 +/- 12.5%, before and after treatment respectively, p < 0.01), in group II this level remained unchanged. In both groups the percentage of CD19+ B cells decreased (14.7 +/- 9.2% and 8.0 +/- 6.1%, before and after treatment respectively in group I, p < 0.01; 17.4 +/- 12.3% and 11.0 +/- 7.1%, before and after treatment respectively in group II, p < 0.01). Moreover, the percentage of activated T cells (CD25+ cells and HLA-DR+ cells) was reduced in both groups.

Administration, Oral↗

PubMed1994

[Biological properties of interleukin 10].

Interleukin-10 (IL-10) is produced predominantly by T-helper lymphocytes and macrophages. IL-10 inhibits lymphocyte-induced cytokine production (CSIF--cytokine synthesis inhibitory factor), cooperates in B lymphocytes activation as well as macrophages--monocytes deactivation (MDF--macrophage deactivating factor). Due to its immunosuppressive properties IL-10 may be used in therapy of some T-cell induced diseases.

Acquired Immunodeficiency Syndrome↗

PubMed1992

Different capabilities of monocytes from patients with systemic lupus erythematosus and rheumatoid arthritis to induce glycosylation alterations of acute phase proteins in vitro.

The effect of conditioned medium on the biosynthesis and glycosylation profile of acute phase proteins secreted by the human hepatoma cell line Hep G2 was studied. Conditioned medium was prepared from nonactivated [CM-LPS(-)] and ex vivo lipopolysaccharide activated [CM-LPS(+)] monocytes from eight patients with active rheumatoid arthritis (RA), five patients with active systemic lupus erythematosus (SLE), and seven healthy subjects. The biosynthesis of albumin, alpha 1-antichymotrypsin and alpha 1-proteinase inhibitor and the profile of glycosylation of proteinase inhibitor were analysed. CM-LPS(-) from patients with SLE had a similar effect to CM-LPS(-) from healthy subjects. In contrast, CM-LPS(-) from patients with RA had the same effect as CM-LPS(+) from healthy donors. A similar effect to that of CM-LPS(+) of healthy subjects was seen with CM-LPS(+) from patients with SLE and with CM-LPS(+) from patients with RA. The treatment of CM-LPS(+) with antibodies against interleukin 6 neutralised most of its ability to induce changes in the biosynthesis and glycosylation of acute phase proteins. Antibodies to interleukin 1 and tumour necrosis factor alpha had only a limited effect on the ability of CM-LPS(+) to induce changes of albumin and alpha 1-antichymotrypsin syntheses, whereas they had no effect on the biosynthesis and glycosylation of proteinase inhibitor. These results indicate that: (a) monocytes isolated from patients with active SLE and active RA have different capabilities of inducing alterations of acute phase proteins in vitro; (b) ex vivo activation of monocytes from patients with SLE leads to the full induction of its capabilities to change acute phase proteins, whereas the activation of monocytes from patients with RA has no additive effects; and (c) interleukin 6 seems to be a major cytokine involved in the regulation of the glycosylation pattern of acute phase proteins.

Acute-Phase Proteins↗

PubMed1989

The inhibitory effect of theophylline on cell cycle kinetics of human lymphocytes in vitro.

The effect of theophylline (TF) on proliferation of lymphocytes in phytohaemagglutinin (PHA), concanavalin A (Con A) and pokeweed mitogen (PWM) freshly stimulated 3-4 days cultures or of 14-days cultured lymphoblasts was studied. Proliferation was estimated by measurement of incorporation of tritiated thymidine (3H-TdR), and by microscopic analysis of cellular divisions progression up to the 4th generation of cells cultured in presence of 5-bromodeoxyuridine (BrdUrd). The strongest inhibition of proliferation was observed when TF was added at the beginning of the cultures. However, when TF was added for the last 20 h of the cultures, a significant decrease in number of the third (M3) and fourth (M4) generation cells was noted and M3/M4 ratio increased from 6.4 up to 19.1. TF inhibited also incorporation of 3H-TdR into cultured lymphoblasts. The obtained data indicate an inhibitory effect of TF both an activation and cell cycle progression of lymphocytes.

Aminophylline↗

PubMedDate not supplied

Does C-reactive protein modulate T-lymphocyte function in methotrexate-treated rheumatoid arthritis patients?

Thirty-four patients with rheumatoid arthritis were treated with oral methotrexate for 6 months. Methotrexate was given as a single weekly dose of 7.5-10 mg. A correlation between serum concentration of CRP and proportion of CD8+ lymphocytes in peripheral blood was found in this group of patients. This correlation can be described by a linear regression equation. According to the results obtained, CRP suppresses lymphocyte function in patients with RA. This is the consequence of the stimulating effect on suppressor mechanisms.

Arthritis, Rheumatoid↗