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T Dao

Publications and source records attributed to T Dao.

At least 37 records · Page 2Linked to original sources
PubMed1996

Interferon-gamma-inducing factor, a novel cytokine, enhances Fas ligand-mediated cytotoxicity of murine T helper 1 cells.

Fas ligand (FasL), expressed on activated T cells, plays a central role in regulating the immune response by inducing apoptosis in activated lymphocytes through binding to its receptor, Fas. We report here that a newly discovered cytokine, interferon-gamma-inducing factor (IGIF) (H. Okamura et al., Nature 378, 88, 1995), selectively enhances the FasL-mediated cytotoxicity of cloned murine Th1 cells, but not Th0 or Th2 cells. Anti-IFN-gamma antibody (Ab) did not block the IGIF-induced cytotoxicity of Th1 cells, nor did IFN-alpha, IFN-gamma, or TNF-alpha augment the cytotoxic activity of Th1, thus indicating that this enhanced cytotoxicity of Th1 cells was mediated by IGIF. In addition, IL-12 was also found to enhance the FasL-mediated cytotoxicity of Th1 cells, suggesting that Th1 cells possesses receptors for both cytokines although these cytokines can act via different pathways. The results thus show that IGIF, recently proposed as IL-18, might play a potential role in immunoregulation or in inflammation by augmenting the functional activity of FasL on Th1 cells.

Animals↗
PubMed1995

[Celiac disease in adults revealed by sensory-motor neuropathy].

Central or peripheral nervous system complications are occasionally observed in adult patients with celiac disease. Several mechanisms have been proposed including vitamin deficiency, vascular inflammation and a direct effect of gluten intolerance. Typical nerve fiber damage due to demyelinization has been suggested. We observed a 65-year old woman with a right peroneal nerve palsy superimposed on a diffuse peripheral neuropathy who was found to have folic acid deficiency which in turn led to the diagnosis of adult celiac disease. Electrophysiological and histological studies demonstrated a predominantly demyelinating peripheral neuropathy which responded first to parenteral folic acid supplementation and second to a gluten-free diet. The mechanisms of peripheral nerve damage in adult celiac disease are briefly discussed and the possible role of folic acid deficiency is emphasized.

Aged↗
PubMed1995

Natural human interferon-alpha inhibits the adhesion of a human carcinoma cell line to human vascular endothelium.

The adhesion of cells to the microvascular endothelium is an essential step in the inflammatory response and metastasis. We have found that pretreatment of a human epidermoid carcinoma cell line, KB, with natural human interferon-alpha (IFN-alpha) inhibited the binding of the malignant cells to human umbilical vein endothelial cells (HUVEC) in a dose- and time-dependent manner. As one of several possible mechanisms for this inhibition, the expression of some revelant adhesion molecules on KB cell surfaces was examined after IFN-alpha treatment. Apart from a slight increase in the expression of integrin alpha 4 beta 1 (very late activation antigen 4, VLA-4), no changes in the expression of other adhesion molecules, such as sialyl Lewis X, CD44, and leukocyte function-associated antigen 1 (LFA-1), which is known to be a heterodimer of CD11a and CD18, were observed after treatment with IFN-alpha. In addition, the cell viability of KB was not affected by treatment of the cells with IFN-alpha, although the cell proliferation was markedly inhibited, indicating that the inhibitory effect of IFN-alpha on KB cell binding to vascular endothelium is not a result of a cytotoxic effect of IFN-alpha. Because the metastatic process requires not only the adhesion of tumor cells to vascular endothelium during their extravasation but also proliferation at distant sites, our findings from this in vitro experimental model suggest that IFN-alpha may have a potential inhibitory effect on tumor cell metastasis.

Antineoplastic Agents↗
PubMed1995

Increased plasma levels of human interleukin for DA1.a cells/leukemia inhibitory factor in sepsis correlate with shock and poor prognosis.

Animal study results have suggested a role in sepsis for human interleukin for DA1.a cells/leukemia inhibitory factor (HILDA/LIF). HILDA/LIF and interleukin-6 (IL-6) levels were prospectively studied by serial ELISAs in 34 septic patients. HILDA/LIF was detected in 11 of 34 patients at plasma levels of 100-37,000 pg/mL. Peak HILDA/LIF levels correlated with increased temperature and creatinine and IL-6 and with decreased arterial CO2 (P < .05). Multivariate analysis showed that shock and decreased arterial CO2 accounted for 75% of peak HILDA/LIF plasma variations (R2 = .753). Fatal outcome was most often associated with detectable HILDA/LIF (> 56 pg/mL) and peak IL-6 plasma levels > 850 pg/mL (sensitivity, 83%; specificity, 87%), but both (at respective levels of > 480 and > 850 pg/mL) were associated with fatal outcome. HILDA/LIF was detected in septic patients exhibiting shock, and its levels correlated with higher mortality and shorter survival.

APACHE↗
PubMed1995

Natural human interferon-alpha enhances the expression of intracellular adhesion molecule-1, integrin alpha 2 and beta 1 by a mucosal epithelial cell line.

We have found that pretreatment of a human oral mucosal epithelial cell line KB with natural human interferon-alpha (IFN-alpha) augments the expression of intercellular adhesion molecule-1 (ICAM-1), and the complex of CD29 and CD49b, which is known as very late antigen (VLA)-2, in a dose-dependent manner, whereas the expression of other adhesion molecules such as CD44 leukocyte function associated antigen-3 (LFA-3), VLA-4 and endothelial leukocyte adhesion molecule-1 (ELAM-1) did not show any significant changes under the same conditions. The pretreatment of KB cells with IFN-alpha also induces the adhesion of these cells to the human leukemia T cell line MOLT-16 and to peripheral T lymphocytes in a dose-dependent manner. However, the adhesion of the above-mentioned T cells to KB cells was not inhibited by specific antibodies against ICAM-1, CD29, and CD49b. The results thus show that adhesion molecules other than ICAM-1, CD29, AND CD49b are responsible for the induced adhesion between T cells and IFN-alpha-pretreated KB cells.

Antigens, CD↗
PubMed1994

T cell determinant structure of myelin basic protein in B10.PL, SJL/J, and their F1S.

Recent experiments have shown that during the course of chronic experimental allergic encephalomyelitis, there is a shift in the determinant hierarchy away from the dominant to other subdominant and cryptic self determinants. It was therefore of interest to define the pattern of dominance for mouse myelin basic protein in the three commonly used experimental allergic encephalomyelitis model strains of mice, i.e., B10.PL, SJL/J, and (SJL x B10.PL)F1. Our studies indicate that many cryptic determinants are demonstrable, which only activate T cells on injection as individual peptides and not with the native protein. The core amino acid residues of the various determinants are defined and range in size between 5 and 10 amino acids. Interestingly, there is a bias toward H-2u-restricted response vis-a-vis the H-2s-restricted response in the (SJL x B10.PL)F1 strain. The TCR V beta 8.2 gene segment was not predominantly used for responses to other determinants, although some B10.PL and (SJL x B10.PL)F1 cell lines expressed V beta 8.2 more than others. This study represents the most comprehensive analysis so far of the pattern of dominant and cryptic proliferative T cell determinants and their core sequences for mouse myelin basic protein.

Amino Acid Sequence↗
PubMed1994

Natural human interferon-alpha augments apoptosis in activated T cell line.

We have previously shown that interferon-alpha (IFN-alpha) augments interleukin-2 (IL-2) production in mitogen-activated but not unstimulated T cells (1). Here, we studied the effect of IFN-alpha on activation-driven cell death (apoptosis) using a human leukemia T cell line, MOLT-16, as a T cell activation model. IFN-alpha alone had no effect on either the IL-2 production or apoptosis of MOLT-16 cells, but significantly increased both the IL-2 production and apoptosis in the MOLT-16 cells after phytohemagglutinin (PHA) stimulation as determined by CTLL-2 assay and by flow cytometric analysis using propidium iodide (PI) staining. Since IL-2 has been shown to induce apoptosis in some systems, we next evaluated whether the apoptosis in MOLT-16 cells was due to endogenous IL-2 production upon PHA stimulation. However, the addition of exogenous IL-2 to unstimulated cultures of MOLT-16 did not induce DNA fragmentation, a characteristic feature of apoptosis, as determined by DNA electrophoresis and by flow cytometric analysis with PI-stained cells. Furthermore, anti-IL-2 antibody did not prevent PHA-induced DNA fragmentation in MOLT-16 cells. Thus, we conclude that both PHA-induced IL-2 production and apoptosis are outcomes of T cell activation and that IFN-alpha may exert immunoregulatory effects on T cell activation by augmenting both processes.

Apoptosis↗
PubMed1994

Interleukin-1 and interferon-alpha augment interleukin-2 (IL-2) production by distinct mechanisms at the IL-2 mRNA level.

The production of interleukin-2 (IL-2) by phytohemaglutinin (PHA)-stimulated cells of human leukemia T cell line MOLT-16 can be significantly increased by interleukin-1 (IL-1) or interferon-alpha (IFN-alpha). The enhancing effect of IL-1 and IFN-alpha on IL-2 production was studied at the IL-2 mRNA level. We show that IL-1 enhances considerably and transiently, with the maximum level between 1 and 2 hr after stimulation, the expression of IL-2 mRNA in the PHA-stimulated cells. The level of IL-2 mRNA declined rapidly within 4 to 6 hr after stimulation in both PHA- and PHA plus IL-1-stimulated cell cultures. On the contrary, IFN-alpha does not elevate the level of IL-2 mRNA above the level in PHA-stimulated cultures, but maintains an enhanced level of IL-2 mRNA in the activated cells for more than 6 hr after stimulation. These observations correlate well with the kinetics of IL-2 protein production into the culture media. The results thus suggest that IL-1 and IFN-alpha may exert an enhancing effect on IL-2 production by distinct mechanisms. In addition, none of the five other lymphokines tested (i.e., IL-2, IL-3, IL-4, IL-5, and IL-6) had any significant effect on IL-2 mRNA expression in the activated MOLT-16 cells.

Cell Line↗
PubMed1994

Effects of direct current on T cell activity: modulation of interleukin-2 production.

The production of interleukin-2 (IL-2) by mitogen-stimulated human peripheral blood leukocytes (PBL) was significantly enhanced by a short pretreatment of PBL with direct current (DC) at low intensities. Exposure of PBL to DC of 1 mA for more than 10 min resulted in inhibition of IL-2 production which correlated with decreased proliferation capacity of the treated cells. DC had similar enhancing and inhibitory effects on IL-2 production by the mitogen-stimulated human leukemia T cell line MOLT-13. However, DC itself did not stimulate IL-2 production in PBL or in MOLT-13 cells. In two additional T cell lines tested, MOLT-16 and H-9, DC did not enhance mitogen-stimulated IL-2 production, but suppressed it when applied at 1 mA for more than 10 min. Both the mitogen-stimulated and the interleukin-1 (IL-1)-enhanced IL-2 production were completely inhibited by 1 mA of DC applied for 20 min. The observed effects of DC were due to a direct action of DC on the cells and not to possible effects of the secondary by-products of electrolysis. These results show that pretreatment of cells with DC can enhance or suppress IL-2 production depending on the intensity of DC and the type of IL-2 producing cell clones.

Electricity↗
PubMed1994

Establishment and characterization of a novel immature T-ALL cell line, UHKT-42, with TCR beta/delta expression.

A novel immature human T-ALL cell line, UHKT-42, was established from a 12 year old male patient with acute undifferentiated leukemia. The cell line expressed surface CD7, CD5 and cytoplasmic CD3 antigens. All other T-lymphocytic antigens were undetectable on the surface or in the cytoplasm of cultured cells. Expression of the T-cell receptor (TCR) beta, TCR delta, CD3 delta and CD3 epsilon genes was detected by Northern blotting in total cellular RNA extracts, however, the expression of TCR alpha and TCR gamma was undetectable. After stimulation by TPA for 3 days, only the appearance of CD25 (Tac antigen) was detected by immunofluorescence and flow cytometry. Secretion of interleukin-2 (IL-2) into the culture media was also detected after stimulation by PHA or TPA, but not in unstimulated cells. These results suggest that UHKT-42 cells are early precursors of T cells, with TCR beta/delta expression.

Antigens, CD↗
PubMed1994

[Palindromic rheumatism disclosing Whipple's disease. Study of 2 personal cases].

Two patients with palindromic rheumatism were diagnosed with Whipple's disease 5 years after onset of the joint symptoms. Twenty-one previously published cases of Whipple's disease with palindromic rheumatism as the first manifestation were identified. Statistically significant differences were found between palindromic rheumatism in patients with and without Whipple's disease. Patients with Whipple's disease were more likely to be male and to exhibit fever and elevated erythrocyte sedimentation rates during joint symptom flares, whereas they were less likely to have involvement of the metacarpophalangeal and proximal interphalangeal joints. None of the patients with Whipple's disease had either skin manifestations of palindromic rheumatism (nodules or paraarthritis) or positive tests for rheumatoid factor. Patients with palindromic rheumatism exhibiting these features should have an intestinal biopsy to look for Whipple's disease.

Arthritis, Rheumatoid↗
PubMed1993

Interleukin-2 production by T cells: a study of the immunoregulatory actions of interferon-alpha, interferon-gamma, and tumor necrosis factor-alpha in phenotypically different T cell clones.

The production of interleukin 2 (IL-2) by phytohemagglutinin (PHA)-stimulated human leukemia T cell lines MOLT-13 and MOLT-14, the T cell receptor (TcR) gamma delta-bearing clones, was significantly increased by adding human natural interferon-gamma (IFN-gamma) to the cell cultures. In addition, the IL-2 production by PHA-stimulated MOLT-13 and MOLT-14 cells was also augmented by human natural tumor necrosis factor-alpha (TNF-alpha) in a dose-dependent manner but was inhibited by IFN-alpha even at low concentrations (10 IU/ml). This pattern of reactivity is different from the responsiveness of the MOLT-16 cells, a TcR alpha beta-bearing cell line, which respond to IFN-alpha and TNF-alpha, but not to IFN-gamma, by augmentation of IL-2 production. These results suggest that (1) the addition of IFN-gamma has a direct effect on PHA-stimulated MOLT-13 and MOLT-14, resulting in an augmentation of IL-2 production; (2) phenotypically different T cell lines vary in their susceptibility to IFN-alpha and IFN-gamma regulation; and (3) the augmentation of IL-2 production by TNF-alpha appears to have no correlation with phenotypically different T cell clones.

Clone Cells↗