Immunoregulatory role in gamma interferon production by a T cell growth factor-dependent experimental malignant glioma-specific cytotoxic T lymphocyte clone

1985 ◽  
Vol 63 (5) ◽  
pp. 763-770 ◽  
Author(s):  
Toshiki Yamasaki ◽  
Hajime Handa ◽  
Junkoh Yamashita ◽  
Yoshihiko Watanabe ◽  
Masaaki Taguchi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Growth ◽  
Malignant Glioma ◽  
T Lymphocyte ◽  
Cytotoxic T Lymphocyte ◽  
Target Cells ◽  
Content Type ◽  
Lymphocyte Clone ◽  
Fine Print ◽  
T Cell Growth Factor

✓ The authors have established a murine malignant glioma-specific cytotoxic T lymphocyte clone (G-CTLL 1) by T cell growth factor (TCGF) using 203-glioma (a methylcholanthrene-induced ependymoblastoma of C57BL/6 mouse origin). The cloned cells were found to release a large amount of gamma interferon (IFN) in response to glioma-associated antigen-specific stimulation. The authors have investigated whether the IFN produced can contribute to killing the target cells. Adding anti-mouse gamma IFN antibody to the mixed clone-target cell culture inhibited IFN production by the cloned cells but the toxicity of the cells was minimally diminished. Therefore, it is suggested that the endogenous gamma IFN produced by the TCGF-dependent cloned cytotoxic T lymphocyte line does not have direct cytotoxic action on the target cells. Furthermore, IFN production as well as cytotoxicity was blocked by anti-Lyt-2 monoclonal antibody in the absence of complement. This suggests that IFN plays a role in the process of antigen recognition of target cells because the Lyt-2 molecule is involved in an antigen-specific function on the cytotoxic T lymphocyte receptor. The role of TCGF in gamma IFN production was also investigated. The spontaneous production of gamma IFN by the cloned cells paralleled the amounts of exogenous TCGF added to the cultures, but TCGF had no synergistic effect on IFN production in the presence of mitogen or tumor antigen. Accordingly, it is possible that TCGF stimulates the cloned cells to proliferate, causing IFN release.

Specific adoptive immunotherapy of malignant glioma with long-term cytotoxic T lymphocyte line expanded in T-cell growth factor

1984 ◽  
Vol 7 (1) ◽  
pp. 37-54 ◽  
Author(s):  
Toshiki Yamasaki ◽  
Hajime Handa ◽  
Junkoh Yamashita ◽  
Yoshihiko Watanabe ◽  
Yuziro Namba ◽  
...  
Keyword(s):  
T Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Malignant Glioma ◽  
T Lymphocyte ◽  
Adoptive Immunotherapy ◽  
Cytotoxic T Lymphocyte ◽  
T Cell Growth ◽  
T Cell Growth Factor

Dynamic changes in viscoelastic properties in cytotoxic T-lymphocyte-mediated killing

1988 ◽  
Vol 91 (2) ◽  
pp. 179-189 ◽  
Author(s):  
K.L. Sung ◽  
L.A. Sung ◽  
M. Crimmins ◽  
S.J. Burakoff ◽  
S. Chien
Keyword(s):  
T Lymphocyte ◽  
Target Cell ◽  
Viscoelastic Properties ◽  
Cytotoxic T Lymphocyte ◽  
Cell Swelling ◽  
Initial Increase ◽  
Target Cells ◽  
Dynamic Changes ◽  
Lymphocyte Clone ◽  
Membrane Cell

The biophysical properties of cytotoxic T lymphocytes during the killing of their target cells was investigated by using a human cytotoxic T lymphocyte clone, F1, and the target cell, JY, for which it is specific. In single cytotoxic cell/target cell pairs after their conjugation there are changes in the viscoelastic properties of the target cell in association with the lethal hit delivery and post-binding cytolytic steps. On the basis of these changes in the target cell, the complex cytolytic event can be divided into stages: the viscoelastic coefficients exhibited an initial increase followed by a return to resting values; thereafter these coefficients decreased below control and then rose again prior to lysis. The eventual killing of the target cell involves bubbling and swelling of the nucleus, clustering of granules, damage to the cytoplasmic membrane, cell swelling, and lysis. The viscoelastic changes involved in target cell death suggest the loss of integrity of its cytoskeletal apparatus.

scholarly journals Monoclonal cytolytic T-cell lines.

1979 ◽  
Vol 149 (1) ◽  
pp. 273-278 ◽  
Author(s):  
P E Baker ◽  
S Gillis ◽  
K A Smith
Keyword(s):  
T Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
T Lymphocytes ◽  
T Lymphocyte ◽  
Cytolytic T Lymphocytes ◽  
Prolonged Culture ◽  
Cytolytic T Lymphocyte ◽  
T Cell Lines ◽  
T Cell Growth Factor

Monospecific cloned cytolytic T-lymphocyte lines have been created utilizing T-cell growth factor. The clones were found to retain their cytolytic specificity after prolonged culture and monospecific function was demonstrated by subcloning procedures. Thus, detailed studies of the phenotypic and functional characteristics of monospecific, homogeneous, cytolytic T lymphocytes will now be possible.

scholarly journals Characterization of soluble factors that induce the cytolytic activity and the expression of T cell growth factor receptors of a T cell hybrid.

1984 ◽  
Vol 160 (2) ◽  
pp. 584-599 ◽  
Author(s):  
F Erard ◽  
P Corthesy ◽  
K A Smith ◽  
W Fiers ◽  
A Conzelmann ◽  
...  
Keyword(s):  
T Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Cell Hybrid ◽  
High Performance ◽  
Apparent Molecular Weight ◽  
Cytolytic Activity ◽  
Target Cells ◽  
T Cell Growth ◽  
T Cell Growth Factor

A rat X mouse T cell hybrid (PC60) proliferates in the absence of T cell growth factor (TCGF) and its cytolytic activity can be induced by culture in mixed leukocyte culture supernatants or concanavalin A-activated rat spleen cell supernatant (CS) to lyse 51Cr-labeled tumor target cells. To characterize the factor(s) responsible for this reversible induction, serum-free CS was fractionated by reverse phase high performance liquid chromatography and by phenyl-Sepharose chromatography. A cytotoxicity-inducing activity (CIA) was separated from TCGF and macrophage-activating factor/interferon-gamma. CIA was found to be a macromolecule with an apparent molecular weight of 12,000-18,000 and a pI of 5.0 and 6.2. Its activity on PC60 cells depended on the addition of TCGF. Thus TCGF may have other effects on T cells than the induction of entry into cell cycle. The number of TCGF surface receptors on PC60 cells was measured using purified 3H-TCGF. TCGF receptors were undetectable on noninduced cells but appeared during induction. The expression of TCGF receptors was not induced either by TCGF or by CIA-containing supernatants or fractions alone, only by a combination of both. These results show that TCGF plays a role in the regulation of the expression of its own receptors.

Establishment of experimental malignant glioma-specific cytotoxic T lymphocyte clone by T cell growth factor

1984 ◽  
Vol 60 (5) ◽  
pp. 998-1004 ◽  
Author(s):  
Toshiki Yamasaki ◽  
Hajime Handa ◽  
Junkoh Yamashita ◽  
Yuziro Namba ◽  
Yoshihiko Watanabe ◽  
...  
Keyword(s):  
T Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
T Lymphocytes ◽  
Cytotoxic Activity ◽  
Content Type ◽  
Tumor Bearing ◽  
Immune Interferon ◽  
T Cell Growth ◽  
T Cell Growth Factor

✓ In an attempt to facilitate the long-term proliferative growth and subsequent cloning of cytotoxic T lymphocytes (CTL's) against syngeneic murine 203-glioma (20-methylcholanthrene-induced ependymoblastoma of C57BL/6 mouse origin), sensitized T lymphocytes from tumor-bearing mice were cultured in the presence of T cell growth factor (TCGF). Of five clones established by a limiting dilution technique, two clones (G-CTLL 1 and 2) exhibited tumor-specific cytotoxicity. G-CTLL 1 cells, which possessed much higher cytotoxic activity than G-CTLL 2 cells, were further analyzed. G-CTLL 1 cells were maintained in a TCGF-dependent exponential proliferative culture for over 18 months and continued to mediate an extremely high cytotoxic activity with the target specificity (50- to 100-fold increases over the peak cytotoxic activity of sensitized T lymphocytes in tumor-bearing mice). Their phenotypes of surface antigens were Thy-1+ (weak positive), Lyt-1.−2.+3+, and asialo-GM1−, and their cytotoxicity was blocked by adding only anti-Lyt-2 monoclonal antibodies. These results indicated that the cloned cells originated from CTL's. The cloned cells were characterized by the production of immune interferon with the glioma antigen-stimulation, suggesting that the immune interferon could enhance the cytotoxic activity of the CTL clone at the site of a clone-target cell recognition event.

Inhibition of proliferation of human cerebral meningioma cells by suramin: effects on cell growth, cell cycle phases, extracellular growth factors, and PDGF-BB autocrine growth loop

1995 ◽  
Vol 82 (4) ◽  
pp. 600-607 ◽  
Author(s):  
Uwe M. H. Schrell ◽  
Stefan Gauer ◽  
Franklin Kiesewetter ◽  
Andreas Bickel ◽  
Jürgen Hren ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Growth Factors ◽  
Growth Factor ◽  
Cell Growth ◽  
Content Type ◽  
Igf I ◽  
Meningioma Cell ◽  
Autocrine Loops ◽  
Fine Print

✓ The growth of human cerebral meningiomas depends on various growth factors, including epidermal growth factor (EGF), transforming growth factor (TGF)-α and TGF-β, platelet-derived growth factor (PDGF)-BB, insulin-like growth factor (IGF)-I and IGF-II, and acidic and basic fibroblast growth factors. The latter three have been shown to form autocrine loops that are thought to be a major component of uncontrolled growth in meningioma tissue. Suramin is known to prevent binding of a variety of growth factors to their receptors in mammalian tissue, thus abolishing para- and/or autocrine-mediated cell growth. The authors therefore tested the effect of suramin on the proliferation of cultured human meningioma cells. Suramin (10−5 to 10−4 M) significantly inhibited the growth of meningioma cells in culture. The maximum effect observed was with the higher dose (10−4 M), which resulted in a 40% to 70% reduction in cellular proliferation. This effect was observed in all 15 tumor samples studied and was confirmed by [3H]thymidine uptake. In studies using DNA flow cytometry, suramin inhibited meningioma cell proliferation in five tumor samples by arresting cells in the S and G2/M phases of the cell cycle. Growth factor (EGF, IGF-I, and PDGF-BB)—induced cell proliferation was completely abolished in five tumor samples when 10−4 M suramin was applied to meningioma cells. Western blot analysis of three tumor samples showed that the intracellular PDGF-BB content of meningioma cells was significantly reduced after treating the cells with 10−4 M suramin. Binding of iodinated growth factors (that is, [125I]EGF, [125I]IGF-I, and [125I]PDGF-BB) to their receptor sites was prevented by suramin in a dose-dependent manner in 10 meningioma membrane fractions. Lowering of the intracellular PDGF content and prevention of extracellular growth factor receptor binding demonstrates that suramin disrupts autocrine loops and paracrine growth stimulation in meningioma tissue. These data provide evidence that growth of cerebral meningiomas in culture is strongly inhibited by suramin at a concentration of 10−4 M. Suramin acts as a scavenger neutralizing exogenous growth factors; thus it can interrupt autocrine loops and paracrine stimulation of human meningioma cell growth. The evidence favors suramin as a therapeutic option for controlling meningioma proliferation in patients with inoperable and recurrent high-grade meningiomas.

Glioblastoma multiforme at the site of metal splinter injury: a coincidence?

1999 ◽  
Vol 91 (6) ◽  
pp. 1041-1044 ◽  
Author(s):  
Michael Sabel ◽  
Jörg Felsberg ◽  
Martina Messing-Jünger ◽  
Eva Neuen-Jacob ◽  
Jürgen Piek
Keyword(s):  
Brain Tumor ◽  
Glioblastoma Multiforme ◽  
Malignant Glioma ◽  
Causal Relationship ◽  
Propionibacterium Acnes ◽  
Glioma Tissue ◽  
Left Frontal Lobe ◽  
Content Type ◽  
Chronic Abscess ◽  
Fine Print

✓ The authors report the case of a man who had suffered a penetrating metal splinter injury to the left frontal lobe at 18 years of age. Thirty-seven years later the patient developed a left-sided frontal tumor at the precise site of the meningocerebral scar and posttraumatic defect. Histological examination confirmed a glioblastoma multiforme adjacent to the dural scar and metal splinters. In addition, a chronic abscess from which Propionibacterium acnes was isolated was found within the glioma tissue. The temporal and local association of metal splinter injury with chronic abscess, scar formation, and malignant glioma is highly suggestive of a causal relationship between trauma and the development of a malignant brain tumor.

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