Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.1.1.148 (Thy1)
 1,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to investigate the influence of oral administration of OK-432 on the tumor growth of tumor-bearing mice. In addition, the changing pattern of the splenic lymphocyte subsets of tumor-bearing mice was evaluated by flow cytometry. OK-432 at a dose of 0.1, 1 or 10 KE was administered orally every 3 days or every other day for 30 days to subcutaneously Meth A tumor-inoculated mice. The tumor growth was significantly inhibited in the 1 KE every 3 days group, in the 1 KE every other day group and in the 10 KE every 3 days group. In the 10 KE every other day group, OK-432 inhibited the tumor growth on days 10 and 20, while the agent did not show a marked inhibitory effect on day 30. The percentages of splenic L3T4-positive cells and splenic asialo GM1-positive cells were significantly increased in the 1 KE every other day group, while the Lyt2+/Thy1.2+ ratio was decreased. On the other hand, in the 10 KE every other day group, OK-432 showed no effect on the percentages of splenic L3T4-positive cells and Lyt2+/Thy1.2+ ratio on days 20 and 30. Our results suggest that the antitumor effect of oral administration of OK-432 may be correlated with the changing pattern of L3T4-positive cells and Lyt2+/Thy1.2+ ratio.
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PMID:The changing pattern of the splenic lymphocyte subsets in tumor-bearing mice after oral treatment with OK-432. 135 56

More than 80% of BALB/c mice bearing BAMC-1 ascites tumor were completely cured after five consecutive (once every 2 days) i.p. injections of a 0.1 mg dose of OK-432, beginning on day 2 after tumor implantation. The antitumor effect of OK-432 was abolished in athymic nu/nu mice and in anti-thymocyte globulin-treated euthymic BALB/c mice, so although OK-432 treatment did increase the length of survival, all animals eventually died as a result of tumor growth. When peritoneal exudate cells (PEC), obtained on day 12 from OK-432-treated BAMC-1-bearing euthymic mice were evaluated for in vivo tumor neutralization activity, all mice receiving an i.p. injection of the admixture of the nonadherent PEC (1 X 10(7) cells) with BAMC-1 cells (1 X 10(5)) survived for more than 60 days. When the same nonadherent PEC (1 X 10(7) cells) were i.p. transferred adoptively 1 day after the inoculation of 1 X 10(5) BAMC-1 tumor cells, again all mice survived. When these in vivo active PEC were tested for cytotoxicity in vitro against fresh BAMC-1 tumor cells, natural killer (NK) sensitive syngeneic RL male 1, NK-sensitive allogeneic YAC-1 cells, NK-resistant syngeneic Meth-A cells, allogeneic tumor cells (EL4, B16, and P815) and xenogenic human cells, the PEC were found to be capable of lysing BAMC-1 tumor cells together with almost all of the other tumor cells, including NK-resistant cells. Nonadherent PEC contained at least two subpopulations of killer cells. One, directed to syngeneic BAMC-1 cells, was both Thy1.2 and asialo GM1 positive, and another, directed to allogeneic YAC-1 cells, was asialo GM1 positive but Thy1.2 negative. A cold target inhibition assay also suggested the presence of more than two subpopulations. These results indicate that T cells play a determined role in the immunotherapeutic effect of OK-432 on BALB/c mice bearing BAMC-1 tumor, although the participation of activated macrophages could not be excluded. The cells responsible for killing BAMC-1 and other tumor cells appearing in the PEC on day 12 were characterized as containing at least two kinds of lymphokine-activated killer cells.
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PMID:Pronounced antitumor effect of LAK-like cells induced in the peritoneal cavity of mice after intraperitoneal injection of OK-432, a killed streptococcal preparation. 242 68

Inflammatory cells were isolated from West Nile virus (WNV)-infected CBA/H (H-2k) mouse brains, and their function and cell surface markers were studied. Two populations of cytolytic lymphocytes were detected. One population, which lysed WNV-infected and uninfected L929 (H-2k), YAC-1 (H-2a), P815 (H-2d), OH (H-2KdDk) and 2R (H-2KkDb) target cells, had a phenotype of L3T4- Lyt2- Thy1 +/- asialo GM1+ and hence were natural killer (NK) cells. The other, which lysed WNV-infected cells to a greater extent than uninfected L929 cells, had a phenotype of L3T4- Lyt2+ Thy1+ asialo GM1- and were cytotoxic T cells. In addition, the presence of the latter population was demonstrated by the specific lysis of syngeneic WNV-infected astrocytes, a cell type which is resistant to NK cell lysis. The cell surface markers of isolated inflammatory cells were determined by two colour flow cytometry. This showed that 15 to 40% of the cells were Thy1+, among which about 3% were Lyt2+. No L3T4+ cells were detected.
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PMID:Identification of cytolytic lymphocytes in West Nile virus-infected murine central nervous system. 254 51

In confirmation of previous reports, we observed lysis of mouse hepatitis virus (MHV)-infected target cells in the presence of spleen and lymph node cells from nonimmunized mice possessing a B cell surface phenotype (IgM+, IgG+, J11d+, Ia+, Fc+, Thy1-, MAC-1- and asialo-GM1-). Lysis was inhibited by MHV-specific antisera. The presence of immunoglobulin at the surface of B cells is not required for cytolysis since MHV-infected target cells are lysed in the presence of the B cell hybridoma Sp2/0, which fails to synthesize immunoglobulin. Using 51Cr-labelled Sp2/0 cells, both target and effector cells were shown to undergo cytolysis. Direct observation of target and effector cells co-incubated after labelling with different fluorescent dyes demonstrated that lysis correlates with the fusion of B cells and MHV-infected cells. These findings are consistent with the idea that the E2 protein of MHV, which is expressed on the infected cell surface and has receptor and membrane-fusion activities at neutral pH, selectively mediates fusion with cells of B lymphocyte lineage. This may represent a general mechanism by which enveloped viruses with fusion proteins that function at neutral pH can interfere with the function of subsets of immune cells.
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PMID:Target and effector cell fusion accounts for B lymphocyte-mediated lysis of mouse hepatitis virus-infected cells. 254 86

We induced nonspecific killer cells in the local site of delayed-type hypersensitivity against keyhole limpet hemocyanin or ovalbumin. Delayed-type hypersensitivity was induced in the peritoneal cavities of mice, and peritoneal exudate cells (PEC) were collected. These PEC were found to have killer activity toward SP2 and YAC-1 cells (target cells susceptible to natural killer cells) by 4-h 51Cr-release assays. The induction of killer activity in PEC was observed in parallel with the eliciting of delayed-type hypersensitivity in the peritoneal cavity, in which the killer activity was maximum 24-48 h after the antigen challenge, but was not induced in nu/nu mice and was induced in an antigen-specific way. These killer cells did not adhere to nylon wool and had Thy1 and asialo-GM1 antigens on their surfaces. Their precursor cells were also asialo-GM1-positive. These findings indicate that the killer cells probably belong to the NK cell lineage. Results of tumor challenge experiments showed that these killer cells had an antitumor effect in vivo as well as in vitro.
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PMID:Induction of nonspecific killer cells by delayed-type hypersensitivity against soluble protein antigens in murine peritoneal cavities. 256 10

We have previously demonstrated that incubation of murine cells in vitro in interleukin 2 (IL-2) induced antibody-dependent cellular cytotoxicity (ADCC) and that these cells were derived from the NK/LAK, FcR+ cell population. In the present study we show that in vivo administration of IL-2 to mice induces cells which exhibit ADCC activity in the peritoneal cavity, liver, lungs, and to a lesser degree in the bone marrow, spleen, mesenteric lymph nodes, and thymus. A gradual increase in ADCC activity and the number of Fc-receptor-positive cells was seen 1 to 3 days after starting IL-2 treatment. The cells mediating ADCC are closely related to LAK cells since they expressed Thy1.2 antigens and are derived from asialo GM1-positive, Lyt2/L3T4-negative, radiosensitive cells. These results demonstrate that IL-2 can systemically induce cells with ADCC activity and that this ability may be useful in the establishment of therapeutic models against disseminated cancer when combined with specific antitumor monoclonal antibodies.
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PMID:Systemic induction of cells mediating antibody-dependent cellular cytotoxicity following administration of interleukin 2. 257 25

Metastasis can be inhibited by asialo-GM1-positive spleen cells, and in this paper we show that there are two such spleen cell populations. One population is adherent and non-cytotoxic to YAC cells, whereas the other population is non-adherent and cytotoxic to YAC cells. Both cell populations exert an antimetastatic activity in cyclophosphamide-treated mice that are inoculated with LL2 Lewis lung carcinoma cells. We conclude that the antimetastatic activity is not only exerted by cytotoxic asialo-GM1-positive cells (apparently natural killer cells), but also by adherent, non-cytotoxic asialo-GM1+, Thy1.2-, IgG- cells. This means that the latter exert their antimetastatic activity by a non-cytotoxic mechanism.
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PMID:Non-cytotoxic asialo-GM1-positive cells exert antimetastatic activity. 259 76

The antitumor mechanism of recombinant human interleukin-2 (rIL-2) was studied using two murine tumor systems. Meth 8 tumor cells were easily lysed in vitro by rIL-2-activated killer (AK) cells, which mainly consisted of Thy1.2+, Lyt2.2+, L3T4- T cells, and asialo GM1+ natural killer (NK) cells; on the other hand, X5563 tumor cells were only slightly lysed in vitro by AK cells under the same conditions. One of these two tumors was inoculated i.d. into C3H/HeN mice and then rIL-2 (5 X 10(4) J.U./mouse/day) was repeatedly injected s.c. For AK-sensitive Meth 8-bearing mice, rIL-2 therapy starting 1 day after tumor inoculation was more effective for the growth than the therapy starting 7 days later and the therapeutic effect was abrogated by in vivo treatment with anti-asialo-GM1 serum. In contrast, for mice bearing AK-resistant X5563 tumor cells, delayed administration starting on day 7 or later was more beneficial than earlier administration on day 1 or 4. This treatment schedule resulted in complete tumor regression in a dose-dependent manner including significant inhibition of metastases in the spleen and/or lymph nodes. These therapeutic effects of rIL-2 on X5563 were not seen in T-depleted mice with anti-mouse thymocyte serum but were found in NK-depleted mice upon treatment with anti-asialo-GM1 serum. The results of these studies showed that the growth of AK-sensitive Meth 8 tumor was inhibited by AK cells, while the growth and metastases of AK-resistant X5563 tumor was inhibited by tumor-specific T cells, which were generated after tumor development and activated by rIL-2 therapy, rather than AK cells.
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PMID:Distinct antitumor mechanisms of recombinant interleukin-2 on recombinant interleukin-2-activated killer-sensitive and -resistant murine tumors. 260 Jun 5

Localized treatment with recombinant human interleukin-2 (rIL-2) +/- recombinant murine interferon-gamma (rIFN-gamma) results in regression of early B16 melanomas in normal C57BL/6 (B6) mice, but not in syngeneic beige mice, which have defective natural killer (NK) cells. Injection of antibodies to asialo GM1 (a-AGM1) or Thy1 abolishes the tymoricidal effects of rIL-1 +/- rIFN-gamma. Thus, cells activated by these cytokines must be either NK-like cells that are AGM1+ Thy1+, or NK-like cells (AGM1+) cooperating with T lymphocytes (Thy1+), since either antibody (a-AGM1 or a-Thy1) independently abrogates the in vivo antitumor effect.
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PMID:In vivo requirement for asialo GM1 and Thy1 positive leukocytes for antitumor effect of rIL-2 +/- rIFN-gamma. 290 82

Mice were injected intravenously with rabbit antiserum to ganglio-n-tetraosylceramide (asialo GM1, ASGM1), a neutral glycosphingolipid present at high quantities on the surface of natural killer (NK) cells. Spleen cells prepared from the mice were then examined for NK activity against YAC-1 targets, for phagocytic cells and by flow cytometric analysis for Thy1, Lyt1, Lyt2, ASGM1 and surface Ig (SIg) phenotypes. Administration of anti-ASGM1 in mice resulted in a complete depletion of NK activity and ASGM+1 cells in the spleen, but no changes in the proportions of Thy1+ cells and their Lyt1+ and Lyt2+ subsets and phagocytic cells. Corresponding to this selective depletion of ASGM+1 cells and NK activity, the spleen cells showed an increased number of SIg+ B cells and augmented mitogenic responses to B-cell but not T-cell mitogens. These NK-depleted spleen cells also showed production of pokeweek mitogen (PWM)-driven plaque-forming cells (PFC) to much higher levels than those of control spleens. In the spleens of mice treated with varying concentrations of anti-ASGM+1, a good correlation was found between the decreased NK activity and the enhanced PFC response. To directly test the possible suppressor activity of NK cells on PWM-induced PFC response, NK (ASGM+1) cells were highly purified from the spleen by a combination of Percoll gradients and cytolysis of T cells by monoclonal antibodies followed by indirect panning. When added to NK-depleted spleen cells, they suppressed the augmented PFC response of NK-depleted spleen cells, depending on the number of cells added. These results suggest that NK (ASGM+1) cells in mice exhibit a suppressor property on B cells, which are undergoing spontaneous or mitogen-induced differentiation.
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PMID:Suppression of B-cell differentiation by natural killer (asialo GM1+) cells in mice. 348 16


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