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E Kontny

Publications and source records attributed to E Kontny.

28 records · Page 2Linked to original sources

Surface markers on human activated T lymphocytes. IV. Comparison of high-affinity E-rosette receptor expression with the expression of other activation markers (receptor for interleukin 2, MHC class II (antigens).

In order to re-examine the value of high-affinity E rosette receptor (Eh-R) as an activation marker of human T lymphocytes, its existence on resting and activated T cells was compared with the expression of such known activation markers as receptor for interleukin 2 (IL-2R; Tac antigen) and MHC class II antigens (DR/DP and DQ). To this aim expression of the above surface markers on lymphocytes of TEe subset, derived from early E rosettes (Eh-R+) and on lymphocytes of TEl subset, derived from late E rosettes (Eh-R-), was examined immediately after purification of the cells from peripheral blood as well as during cell activation with PHA. The phenotypic studies were done by using monoclonal antibodies and indirect immunofluorescence technique. We confirmed previous observation that in the course of PHA stimulation Eh-R like IL-2R marked currently activated T cells. However, it was also found that in the long-term cultures of lymphocytes activated with PHA, the expression of Eh-R was sustained on the cells which lost their IL-2R and DR/DP antigens. The above findings and the fact that TEe cell subset consisting of Eh-R+ lymphocytes was almost completely depleted from cells bearing IL-2R and MHC class II antigens allowed us to conclude that this subset of peripheral blood T lymphocytes represented not currently activated cells but the cells which had been previously activated in vivo.

Antigens, Differentiation, T-Lymphocyte↗

Surface markers on human activated T lymphocytes. III. High-affinity E-rosette receptors.

High-affinity E-rosette receptor (EhR) is suggested to be an activation marker of human T lymphocytes. The present study has been undertaken to estimate the dependence of EhR expression upon the T cell activation. To this aim the expression of EhR on T cells stimulated with PHA was examined. Nonsynchronized and arrested in G1 phase of cell cycle cultures of T lymphocytes were employed. The kinetics of expression of either de novo induced or reexpressed EhR was estimated by using two T cell subsets (originally EhR- and EhR+). In accordance with opinion of others, our results have shown that EhR is an activation marker of human T cells. Moreover, we have found that EhR is the marker of early and late activation stage because: its expression is induced in G1 phase of cell cycle, it continues to increase with the time of mitogen stimulation and the maximal level of EhR expression coincides with the time of the maximal RNA and DNA synthesis. Both induced de novo and reexpressed Eh receptors display the same expression kinetics.

Antigens, Differentiation↗

Surface markers on human activated T lymphocytes. II. CD4 and CD8 differentiation antigens.

In order to estimate the dependence of CD4 and CD8 antigen expression upon the cell activation, their presence on resting and activated human T cells was investigated. Peripheral blood lymphocytes of healthy donors derived from late (TEl) and early (TEe) E rosettes were used as resting and presumably in vivo activated T cell subsets, respectively. Expression of the above markers on T cells stimulated in vitro with PHA was also examined. It was found that both lymphocyte subsets contained similar percentage of CD4+ cells, nevertheless, TEe subset was partially enriched in CD8+ cells. PHA stimulation induced in TEe and TEl subsets the considerable increase of proportion of phenotypical opposing cells, CD8+ or CD4+, respectively. The above changes coincided with the time of the maximal DNA synthesis (the 72nd h of cell stimulation).

Antigens, Differentiation↗

Surface markers on human activated T lymphocytes. I. Fc receptors for IgG and IgM.

Expression of Fc gamma and Fc mu receptors on human peripheral blood T lymphocytes of two subsets with high (E early rosette forming presumably in vivo activated cells, TEe) and low affinity of E receptors (E late rosette forming presumable resting cells, TEl) was investigated. Different distribution pattern of T gamma and T mu cells in the both examined T cell subsets was found. Thus TEe and TEl subsets have been partially enriched in T mu and T gamma cells, respectively. Furthermore, the results obtained in the PHA-stimulated system have shown that Fc mu receptors do not function as the markers of T cell activation. However, in opposition to this finding Fc gamma receptors may be the early activation markers but only of T cells originally bearing high-affinity E receptors.

Antigens, Differentiation↗

The effect of taurine chloramine on pro-inflammatory cytokine production by peripheral blood mononuclear cells isolated from rheumatoid arthritis and osteoarthritis patients.

OBJECTIVE: Pro-inflammatory cytokines play a critical role in the pathogenesis of RA. A natural oxidant, TauCl exerts anti-inflammatory activities. Here, the effects of Tau and TauCl on key pro-inflammatory cytokines--IL-1beta, IL-6 and TNF-alpha production by LPS-triggered peripheral blood mononuclear cells (PBMCs) isolated from RA and OA patients and healthy blood donors--were examined. METHODS: PBMCs were stimulated with LPS (24 h) in the presence of Tau or TauCl (200-400 microM). Cytokine production was measured in culture supernatants (secreted) and cells lysates (cell-associated) using specific ELISAs. RESULTS: Production of the secretedforms of IL-1beta and IL-6 was inhibited by TauCl with IC50 approximately equal to 250 microM and 300-400 microM respectively, in all investigated groups. In all cultures of PBMCs TauCl raised the TNF-alpha production at the low concentration (200 mM), while at the higher concentration (400 microM) either reduced it (55% of RA, 70% of OA patients and 55% of healthy donors) or exerted no effect (remainder of patients). Interestingly, Tau did not significantly affect any cytokine production. CONCLUSION: TauCl at high concentrations down-regulates pro-inflammatory cytokine production. However, the impact of TauCl on TNF-alpha production by PBMCs from RA is more limited than in cells isolated from OA patients.

Adult↗

Modified expression of c-Fos and c-Jun proteins and production of interleukin-1 beta in patients with rheumatoid arthritis.

OBJECTIVE: To examine the relationship between the expression of c-Fos and c-Jun proteins and the METHODS: The expression of c-Fos and c-Jun proteins and the production of IL-1 beta in the PBMC of 11 patients with active RA was determine by Western blots and ELISA techniques, respectively. RESULTS: The spontaneous expression of c-Fos protein and the production of IL-1 beta was higher in RA patients. Under LPS treatment, the PBMC of both RA patients and healthy subjects produced similar high levels of IL-1 beta without any significant changes in the expression of c-Fos and c-Jun proteins. By contrast, PMA-induced production of IL-1 beta was impaired in RA patients and was preceded by the disregulated expression of c-Fos and c-Jun proteins when compared with healthy donors. CONCLUSION: It can be postulated that in some RA patients the spontaneously high production of IL-1 beta may be associated with the up-regulated expression of c-Fos protein in PBMC. On the other hand the impairment of IL-1 beta production in RA induced by the PKC-dependent pathway, may be related to disturbances in c-Fos and c-Jun protein expression. This dysfunction seems to be compensated by some unknown mechanisms implicated in LPS signalling, which is known to involve not only the PKC-mediated pathway.

Aged↗