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Results for “Mast-Cell Sarcoma”

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At least 19 recordsLinked to original sources
PubMed1975

Correlation of "sneaking through" of tumor cells with specific immunological impairment of the host.

The preferential take of tumors after small-size inocula of transplantable tumor cells has been described for many systems. The phenomenon has been named "sneaking through" or "dilution escape". Using a BALB/c mastocytoma, we have analyzed the immunological parameters accompanying sneaking through that can be observed upon injection of 10(1) to 10(3) living cells. Mice can also be conditioned by injection of low, subimmunogenic numbers of irradiated cells to show increased tumor incidences upon injection of living cells in doses two orders of magnitude above the sneaking through dose. The general immune reactivity of the animals is not impaired under these conditions. However, determinant-specific unresponsiveness is found which can be transferred by spleen cells and therefore seems to be actively maintained. It is concluded that sneaking through of tumor cells is the result of specific immunological impairment of the host's immune system by subimmunogenic small-size inocula of tumor cells.

Animals↗
PubMed1977

Failure of T cells specific for strong histocompatibility antigens to cooperate with B cells for a humoral response.

Thymus-derived lymphocytes (T cells) selected for reactivity to strong histocompatibility antigens over a period of one to twelve months in vitro were tested for their ability to cooperate with bone marrow-derived lymphocytes (B cells) for a humoral response. If cultured with normal syngeneic or allogeneic spleen cells and sheep erythrocytes (SRBC) as immunogen, inhibition of the anti-SRBC response was observed. Similarly, in T cell-free spleen cells the alloreactive T cells did not stimulate a humoral response, indicating that they cannot exert cooperative activity on B cells. Since it was possible that the alloreactive T cells may cooperate with B cells in a humoral response to immunogens carrying histocompatibility antigens, hapten-coupled tumor cells were also used as immunogen. Though it is demonstrated that the alloreactive T cells do recognize the tumor cell immunogen, no stimulation of the B cells for a humoral response against the tumor cell is observed. This result, as well as the finding that the antigenic requirements for T helper cell priming and cell proliferation of the alloreactive T cells are different, suggests that these alloreactive T cells and helper T cells belong to different T cell subsets.

Animals↗
PubMed1975

Inhibition of sensitization of T-cells by alpha-fetoprotein.

A two-phase model of allograft immunity was studied. In the first phase, specific immune T-cells were generated by incubation of responder cells with mitomycin-C treated allogeneic stimulator cells of the same H-2 type as mouse mastocytoma tumor cells. In the second step, the ability of the sensitized cells to kill Cr51-labelled P-815 mastocytoma cells was assayed. Alpha-fetoprotein (AFP) was shown to inhibit the generation of immune cytotoxic T-cells at low concentrations (1-100 ng/ml) when added at the beginning of the first phase. When added at the end of the first phase or in the second (killing) phase, AFP was found to have no significant effect on cytotoxicity, indicating that it did not inhibit the killer T-cell once it was generated.

Animals↗
PubMed1977

The modulation of histamine release by alpha-adrenoceptors: evidences in murine neoplastic mast cells.

Murine neoplastic mast cells which have been loaded with exogenous labelled histamine, released 14C-histamine when exposed to increasing concentrations of phenylephrine and noradrenaline. Adrenaline was only slightly effective, while isoprenaline and dibutyryl-cyclic-AMP were fully inactive. The release of histamine evoked by alpha-adrenergic agonists was antagonized by phentolamine, and left unchanged by practolol and cocaine. It is concluded that alpha-adrenoceptors may be valuable in evoking histamine release by murine neoplastic mast cells.

Animals↗
PubMed1976

Activation of fibroblast procollagenase by mast cell proteases.

Proteases capable of activating procollagenase from gingiva and from fibroblast and macrophage monolayer cultures were harvested from homogenates of canine tumor mast cells. The mast cell proteases lysed casein and Azocoll but not native collagen. In low salt concentrations the enzymes existed at high molecular weight complexes, which were dissociated by increasing the salt concentration above 1.0 M (NaCl, KCl). Gel filtration in 1.4 M KCl separated the protease activity into three peaks, all of which activated procollagenase. Two of the enzymes showed substrate specificities (hydrolysis of p-tosyl-L-arginine methyl ester and benzoyl-tyrosine ethyl ester) and reactive center reactivities similar to pancreatic trypsin and chymotrypsin. Based on gel filtration, apparent molecular weights of 160 000 (p-tosyl-L-arginine methyl ester esterase), 90 000 (main procollagenase activator) and 36 000 benzoyl-tyrosine ethyl ester esterase) were determined. Activation of procollagenase resulted in a 18-20 000 decrease of the molecular weight. The activation was directly related to the amount of activator added within certain limits. Further addition of activator resulted in proteolytic inactivation of collagenase.

Animals↗
PubMed1978

Xenogenic response of human peripheral blood lymphocytes against murine cells in vitro.

Human peripheral blood lymphocytes (HPBL) were sensitized to mitomycin-treated murine spleen cells and mitomycin-treated mastocytoma P-815. A DNA proliferative response occurred to both cell types. The sensitized HPBL lysed chromium-51-labelled mastocytoma P-815 cells in a cell-mediated cytotoxicity assay (CMC). Evidence is presented that this human-murine xenogeneic system involves T cell response with specificity in CMC mainly toward H-2 antigens. DBA/2 splenocytes were superior to mastocytoma cells as sensitizers in the xenogeneic DNA proliferative assay.

Animals↗
PubMedDate not supplied

A multiple-parameter comparison of immunocompetence and tumor resistance in aged BALB/c mice.

Several parameters of cell-mediated and humoral immunity were measured in young-adult and aged BALB/c mice and compared with resistance to the ascites form of intraperitoneal induced P815 mastocytoma. It was found that the age-related decline of in vitro phytohemagglutinin (PHA) responsiveness by spleen cells approximated the marked decrease of old mice to tumor-cell challenge and approached that characteristically seen in humoral immunity. Thus, decreased PHA responsiveness of splenic lymphocytes provided as sensitive an estimate of the age-related decline of immunocompetence in old mice as other classical parameters of cell-mediated immunity (e.g. graft-vs-host reaction or in vivo cellular proliferation of parental spleen cells in lethally-irradiated F1 recipients). Results could be interpreted to represent a decreased ability of noncycling T-cells to be released to a functional cycling state.

Aging↗
PubMed1979

Spin labeling studies of the interactions of P815 mouse mastocytoma cells with antiserum to histocompatibility antigens, H-2d.

The effect of antiserum to histocompatibility antigens on the membrane organization of murine neoplastic mast cells (P815) has been studied by spin labeling. Incubation of in vivo passaged cells, labeled with a nitroxide derivative of methyl stearate, with antiserum to membrane carried histocompatibility antigens, H-2d, resulted in an apparent decrease in membrane fluidity that was accompanied by histamine release. This electron spin resonance (esr) detectable change was found to be temperature, time, and dose dependent. Treatment of the cells with cytochalasin B, a drug disrupting microfilament structure, inhibited the effects induced by H-2d antiserum. In contrast, vinblastine, which disrupts microtubules, did not modulate the effect of this antiserum. Other data presented here suggest that some of the large spectral change observed on treatment of the cells with anti-H-2d serum may result from hydrolysis of the spin label fatty acid ester via activation of a membrane-associated esterase. The relationship of these results to other immunologically induced membrane phenomena is discussed.

Animals↗