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[Acute mast-cell leukemia. Cytochemical and ultrastructural study, about a particular case (author's transl)].

A case of acute Mast-cell leukemia was studied. A 39 years old female presenting with a brief history of abdominal pain and attacks of flushing; peripheral blood and bone marrow contained up to 60% of poorly differentiated blasts with clumping of deep purpule granules. Peroxydase reaction stains were negative, chloroacetate esterase were strongly positive. Toluidine blue revealed metachromatic stain. Histamine content of the cells was highly greater than normal but nos heparinoid activity could be demonstrated. These abnormal mast-cells have been investigated with the electron microscope; only the dense particular type of granule substructure was found, without any lamellae component. The cells were temptatively classified as "immature" mast-cell. The disease was interpretated as an acute leukemic variety of systemic mastocytosis.

Acute Disease↗
PubMed1979

Target-effector interaction in the natural killer cell system: isolation of target structures.

A sensitive target binding assay has recently been shown to detect natural killer (NK) cells in the mouse. Preincubation of NK cells with detergent-solubilized cell-surface proteins of YAC lymphoma cells prevented subsequent binding to intact YAC targets. The NK target structures (NK-TS) consisted of three molecular species tentatively assigned molecular weights of 130,000, 160,000, and 240,000 based on electrophoretic mobility in sodium dodecyl sulfate/polyacrylamide gels. Moloney cell surface antigen (MCSA), gp71, p30, H-2, and NK-TS were localized in distinct fractions of gels. The NK-TS bound to concanavalin A-Sepharose columns and could be eluted with the specific sugar, suggesting that the target structures may be glycosylated. NK-TS molecules could not be detected in gels of NK-insensitive target cells such as P815, A9HT, YWA, or EL-4. The quantity obtained from the gels varied directly with the NK sensitivity of YAC which is more sensitive when grown in vitro than when grown in vivo. The NK-TS molecules specifically inhibited the binding of NK cells but not alloimmune T cells to their appropriate targets. Additional NK-sensitive tumor cells also expressed some or all of the target molecules exhibited by YAC. Some of these structures shared specificities in the case of MPC-11 or were unique in the case of Molt-4 and K562, as shown by cross-inhibition studies. These results suggest that NK-sensitive cell lines express distinct target structures with possible relevance to natural tumor resistance.

Animals↗
PubMed1978

Tumor-induced immunosuppression.

Three tumor systems, including a mastocytoma, plasmacytomas, and a leukemia-lymphoma were studied for their ability to modify humoral immunity to sheep erythrocytes both in vivo and in vitro. All tumors resulted in a depression of the hemolytic antibody plaque-forming cell response in susceptible mice. These studies indicated that the mechanism(s) of suppression, although not fully defined, were different for each model system investigated.

Animals↗
PubMed1979

Further characterization of thymic suppressor cells and a factor that suppress the generation of cells cytotoxic for a syngeneic tumor in DBA/2 mice.

Antigen-specific suppressor cells and suppressive extracts obtained from the thymuses of DBA/2 mice bearing small syngeneic P815 mastocytomas were compared for their immunogenetic properties and requirements. The assay for specific suppression involved the ability of either cells or extracts to inhibit the primary in vitro cytotoxic response of normal DBA/2 splenocytes to mitomycin-treated P815 cells. It was shown that pretreatment of suooressor cell populations with anti-Iad antiserum plus rabbit complement removed the suppressive activity. Similarly, absorption of the suppressor factor with anti-Iad antiserum removed the suppressive properties of the material. It was found that the suppressor cells, generated in DBA/2 tumor bearers, were capable of specifically suppressing the anti-P815 response of B6D2 F1 radiation chimeras possessing lymphoid cells of the H-2b or H-2t2 haplotype equally as well as they could suppress the response of H-2d-bearing effector cells. This indicates that the suppressor cells are not H-2 restricted with respect to K or D markers on the responder cells in this system.

Animals↗
PubMed1975

Pepstatin, an inhibitor of leukokinin formation and ascitic fluid accumulation.

Ascites fluid accumulation accompanying a mastocytoma or L1210 murine tumor is significantly retarded following the i.p. or s.c. injection of moderate quantities of pepstatin, a known acid protease inhibitor. No effect on cell count was noted by pepstatin treatment. The probable mechanism by which pepstatin acts is by inhigiting the enzymatic formation of chemical mediators known as leukokinins. These are pharmoacologically active peptiedes having potent permeability characteristics previously described by this laboratory. Leukokinins are formed by cathepsin D-like enzymes present in the invading cells and in the ascites fluid acting on a protein substrate, leukokininogen. present in the ascites fluid. Pestatin inhibits the action of these leukokinin-forming enzymes invitro but has no effect on kallikreins (bradykinin-forming enzymes) in vitro. Human ascites fluid from a patient with ovarian carcioma was found to have a paepstatin-inhibited, leukokinin-generating system, as does the mouse. A 'chemical mediator' theory is proposed for ascites fromation which broadens the previously held theory of lymphatic blockage (Holm-Nielsen) and may explain the recent findings of Hirabayashi and Graham of increased plasma-ascites exchange in peritoneal carcionmatosis. Pepstatin inhibition of chemical mediator formation may represent a new therapeutic approach to ascites fluid accumulation in neoplastic disease.

Animals↗
PubMed1977

Characterization of suppressor cells in mice bearing syngeneic mastocytoma.

Suppressor cells from syngeneic P815 mastocytoma-bearing DBA/2 mice that inhibit in vitro generation of specific anti-tumor cytotoxicity were characterized. Suppressive activity was almost completely eliminated by treating suppressive spleen cells with anti-theta serum and complement. Treatment with anti-mouse lg serum and complement or with carbonyl iron did not affect their suppressive activity. When suppressive thymocytes from P815 tumor-bearing DBA/2 mice were tested for their capacity to inhibit the generation of cytotoxicity against L1210 cells, a leukemia line in DBa/2 mice, they did not affect the activity, indicating that the supressor cells in the thymocytes of P815 tumor-bearing mice are specific to the tumor. When Ficoll-Hypaque density cell separation was carried out with cytotoxic spleen cells and suppressive spleen cells from 815 tumor-bearing mice, the dense fraction was enriched for kiler cells whereas the suppressive activitty was mainly recovered in the light fraction. Therefore, killer cells and suppressor cells in P815 tumor-bearing mice are thought to be distinct populations.

Animals↗
PubMed1978

[Toxoplasmosis transmission by blood transfusion? (author's transl)].

T-cells of the chicken tumour HPRS-1, mouse mastocytoma cells, Friend virus-transformed erythroleukaemia cells as well as normal human, mouse and chick erythrocytes were tested for their receptivity to toxoplasma infection. The studies indicate that T-cells and mastocytoma cells, which may be counted as part of the white blood cell series, have the highest invasion rate after incubation with toxoplasma. Friend-erythroleukaemia cells were less often affected; mature human, mouse and chick erythrocytes were refractory. The results suggest that cells of the white blood cell series are receptive to toxoplasma infection but that nucleated precursors of the red series may also be so, while mature erythrocytes cannot be infected. The possibility of transmission of toxoplasmosis by blood transfusion can no longer be doubted.

Animals↗
PubMed1977

Increased primary cell-mediated immunity in culture subsequent to adriamycin or daunorubicin treatment of spleen donor mice.

Spleen cell populations from mice treated with Adriamycin or daunorubicin were found to develop a greater complement-independent cellular cytotoxic immune response during culture with allogeneic tumor cells than spleen cells from untreated or cyclophosphamide-treated animals. A temporal and drug dose dependence of this effect was demonstrated. The changes in spleen cell population occurring in the donor mice consequent to drug treatment were evident in the nylon woll-adherent fraction of the spleen cells. The results are consistent with the possibility that the concentration of specific progenitor or accessory cells in the spleen is increased consequent to drug treatment.

Animals↗
PubMed1977

In vitro induction of polyclonal killer T cells with 2-mercaptoethanol and the essential role of macrophages in this process.

Killer T cells against allogeneic and syngeneic tumor cells were generated in vitro by the addition of 2-mercaptoethanol (2-ME) to the murine spleen cell culture in the absence of any antigenic stimulation. The maximum activity of T cell-mediated cytotoxicity (CMC) induced with 2-ME was observed on day 4 of culture and the induction of CMC was completely inhibited by the addition of inhibitor of DNA synthesis, hydroxyurea, or cytosin arabinoside. CMC induced with 2-ME was specifically inhibited by the addition of unlabeled target cells to the 51Cr-release assay system. These results indicated that killer T cells were generated in the presence of 2-ME as a result of nonspecific polyclonal activation of precursors into cytotoxic effector cells and that they recognized target cells with antigen-specific recognition receptors. Spleen cells deprived of adherent cells showed impaired induction of CMC with 2-ME. The addition of peritoneal exudate macrophages to splenic T cells restored this response. The result indicated that macrophages were essential for the induction of CMC with 2-ME. The possibility that the function of macrophages was mediated by soluble factor(s) released from macrophages was demonstrated by the separate culture of splenic T cells and macrophages in double-chambered, Marbrook-type vessels and by the addition of supernatants from macrophage cultures to splenic T cells. 2-ME and soluble factor(s) released from macrophages seemed to be required for the activation of precursors into killer cells.

Animals↗
PubMed1977

Specificity of rat xenogeneic cell-mediated cytolysis for the products of the K and D loci of the mouse H-2 complex.

Lewis rat lymph node (LN) cells, when cultured with irradiated mouse spleen cells, develop cytotoxic effectors that were shown to be specific for the sensitizing mouse strain. Alloantisera directed to the products of the K and D loci of the target inhibited cytolysis whereas an antiserum to the I region gene products did not inhibit cytolysis even though LPS-induced spleen blasts were used as targets. Thus, it appears that even when effector cells from another species are generated to mouse spleen cells, the gene products of the K and D loci continue to play a predominant role.

Animals↗
PubMed1977

Arming of macrophages with lymphocytes from mice immunized with tumor tissue.

C57BL/6 macrophages are rendered specifically cytotoxic ("armed") by incubation with spleen cells from C57BL/6 mice sensitized in vivo with allogeneic P-815 mastocytoma cells. Data are presented which suggest that the cytotoxic activity of the macrophages is not due to the adherence of sensitized lymphocytes. The results indicate that it is the T-lymphocyte which is primarily involved in arming. Furthermore it is the cytotoxic and not the proliferating T-cell which is responsible for arming.

Animals↗