Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 72 human leukemia-lymphoma cell lines were studied for reactivity with the monoclonal antibody (MAb) A7, an anti-human colon-cancer-cell-associated antigen reagent, by indirect membrane immunofluorescence. Nine of the 72 cell lines expressed the antigen recognized by A7 MAb. Five of the 34 T-cell lines, 2 of the 21 B-cell lines, and 2 of the 3 non-lymphoid-non-myeloid cell lines were reactive with A7 MAb. By means of SDS-PAGE and immunoblotting, the antigens isolated from both colon cancer cell lines (WiDr, SW1116 and LoVo) and leukemia cell lines (A3/KAWAKAMI, H9, RPMI 8226 and SPI-801) showed an identical MW of 42-43 kDa. The non-glycosylated antigen recognized by A7 MAb, which was expressed on both the colon cancer line (SW1116) and the leukemia line (H9) in the presence of tunicamycin, also showed an identical MW of 36 kDa. However, the quantity of the antigen in the leukemia cells was significantly lower than in the colon cancer cells. Although expression of this colon-cancer-associated antigen in the non-colon cancer cells is real, the significant expression of this antigen in colon-cancer cells makes it useful for clinical monitoring of colon cancer patients.
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PMID:Identification and characterization of a colon-cancer-associated antigen expressed on leukemia-lymphoma cell lines. 199 51

The effect of cold or isolation stress on mortality rate and brain virus level were investigated in mice infected with West Nile virus (WNV). Exposure of mice for 5 min/day to cold water (1 +/- 0.5 degrees C) for 8-10 days resulted in 92% mortality as compared to 47% in control mice (p less than 0.001). Mice housed in individual cages (isolation stress) were also more susceptible to WN viral infection, as shown by increased mortality rate reaching 85% as compared to 50% in mice housed 6 per cage (p less than 0.01). Cold or isolation stress increased blood brain and spleen virus levels as early as 2 days after inoculation. After 8 days of isolation or cold stress, mice inoculated with WNV had 8.9 and 9.0 log10 plaque forming units in the brain, respectively, as compared to 6.9 in the control (p less than 0.01-0.001). Furthermore, lymphoid organs such as spleen and thymus showed severe mass loss. These data suggest that physical or non-physical stress situations enhance WNV encephalitis by accelerating virus proliferation and increase mortality in mice.
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PMID:The influence of cold or isolation stress on resistance of mice to West Nile virus encephalitis. 215 14

The genetically engineered herpes simplex virus strains R7017 and R7020 were tested in owl monkeys (Aotus trivirgatus) previously shown to model herpetic diseases of immunocompromised patients and neonates. In contrast to the lethal disease seen in monkeys receiving 100-1,000 plaque-forming units (pfu) of wild-type virus, inoculation of greater than or equal to 10(6) pfu of recombinant viruses produced local lesions and viral shedding but not disseminated disease. Latent recombinant viruses were recovered from some ganglia innervating the sites of inoculation. Monkeys protected from lethal infection with wild-type virus exhibit recurrent lesions that increase in frequency and severity after total lymphoid gamma irradiation (TLI). In contrast, monkeys immunosuppressed by TLI and inoculated with R7020 could not be differentiated from irradiated controls with respect to morbidity or mortality. Moreover, the virus was not transmitted from immunosuppressed infected females to normal male cage mates.
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PMID:In vivo behavior of genetically engineered herpes simplex viruses R7017 and R7020. II. Studies in immunocompetent and immunosuppressed owl monkeys (Aotus trivirgatus). 216 4

We believe that any questions regarding whether the CNS can alter immune system functions no longer remain. It can conclusively be stated that the immune system is susceptible to influences of the CNS. It remains to be determined whether all classes of lymphocytes, NK cells, macrophages, polymorphonuclear leukocytes, and other antigen-processing cells are all susceptible to CNS influences. We have presented evidence that peripheral blood lymphocytes may not reflect the immunological activity of lymphocytes within lymphatic tissue after being influenced by a stressor. Thus, all types of immunological cells must be evaluated in different organs. Whether the immune system of young and old animals respond in the same way must also be determined. The sex of the animal needs to be taken into consideration. What immune responses are important to measure? Do in vitro responses reflect the ability of an animal to resist infectious disease or susceptibility to autoimmune and malignant diseases? Certainly, absence of an immune response is detrimental to health. It must be determined whether moderately suppressed immune function in multiple compartments is as detrimental as total absence of an immune response in a single immunological compartment. The data that we have presented with respect to adjuvant arthritis indicate that an immune response in the peripheral of the animal can be modified by a stressor and influence an immunopathological process. This may indicate that the most important immune compartment to evaluate with respect to altering disease susceptibility is the peripheral blood and that lymphoid tissue may be interesting, but not clinically relevant. The reasons why the peripheral blood and lymphoid tissue differ in their immunological function following exposure to a stressor must be determined. We have reviewed information indicating that lymphoid tissue is innervated and that such innervation can modify immune function. In addition, hormones released by the CNS may alter immune function. Yet, much of this data are contradictory and whether immune enhancement or suppression occurs is not clearly defined with respect to any experimental manipulation involving denervation or the addition of hormones to in vitro cultures. Whether this reflects the age of the experimental animal, the type of immune response being measured, the adequacy of the experimental procedure, background rearing conditions of the animals, the amount of noise in the animal room, the diet of the animals, or the number of animals housed per cage all remain to be determined. Our purpose has not been to provide a comprehensive review of all of the data relating to the immune system/CNS interaction.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bidirectional interaction between the central nervous system and the immune system. 267 62

We have used immunofluorescence staining with antibodies that detect vimentin, tubulin and the centrioles to compare the distributions of these respective antigens during the division of several suspension and attached cultured cells. Our observations demonstrate that 1) from distinct interphase organizations in suspension and attached cells, the vimentin system consistently rearranges with the onset of mitosis into a filamentous cage-like structure enclosing the spindle, 2) during cytokinesis, the polar centrosomes relocalize near the midbody in suspension cells while they remain at the pole opposite to it in attached cells, and 3) the vimentin cage is disintegrated and aggregated on each side of the midbody during cytokinesis in lymphoid cells but may be retained in other suspension cells.
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PMID:Organization of the vimentin system and its spatial relationship to the microtubule complex during the division of mammalian cells growing attached and in suspension. 275 1

As previously reported for natural killer (NK) cells of normal individuals, prior incubation of peripheral blood lymphocytes from cancer patients with human normal serum or monomeric immunoglobulin G reduced their subsequent capacity to kill K562 target cells in a 4-h 51Cr release assay. The NK activity of such treated effector cells was significantly inhibited only by 58% of sera from patients with colorectal adenocarcinoma (21 of 36 cases) and by 67% of sera from patients with other lymphoid or nonlymphoid solid tumors (22 of 33 cases). The cytotoxic activity of cells previously incubated with eight noninhibitory sera was even augmented relative to medium-treated peripheral blood lymphocytes (control). The 26 untreated cancer sera which did not inhibit significantly the NK activity (I-) always developed significant inhibitory capacity upon heating at 56 degrees C for 30 min (delta+). An additional seven (21%) patients with colorectal carcinoma and four (27%) patients with other cancers were identified as having type II NK regulation, defined as sera with untreated inhibitory capacity (I+) but with appreciably more inhibition after heating (delta+). The sera of the last group of patients with colorectal adenocarcinoma (14 of 36 cases) defined as having type III NK regulation were not different from control sera isolated from normal individuals (I+ delta-) except that they induced an inhibition greater than that caused by normal sera. The modulatory characteristics of sera from the first two categories of patients appear to be cancer associated, since the patterns I- delta+ or I+ delta+ were observed with sera from only one of 30 patients with benign digestive diseases and two of 100 apparently healthy individuals. Preliminary results of longitudinal investigations of patients with colorectal adenocarcinoma revealed also that these patterns disappeared several months after resection of their tumor in all five tested patients, whereas the type III NK regulation found in patients with poor prognostic factors was unchanged after surgery in the other five of six patients. The three different categories of cancer sera identified by the functional assay of NK regulation indicated differences among our group of patients which were not paralleled by differences in levels of cytotoxic reactivity of their NK cells assayed in vitro in the absence of autologous serum.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Modulation of natural killer cell activity by serum from cancer patients: preliminary results of a study of patients with colorectal adenocarcinoma or other types of cancer. 335 20

Of 54 Macaca arctoides, 44 died during the 2.5 years after their assignment to a common cage. Although early deaths were due to trauma, acute gastric dilatation, and shigellosis; latter deaths were the result of a variety of uncommon diseases including atypical mycobacterial disease, malignant lymphoma, protozoan encephalomyelitis, and other necrotizing and inflammatory lesions. Atypical mycobacterial disease due to Mycobacterium avium intracellular serotypes was the most frequent single disease agent recognized (33% [18 macaques]). This disease began in the ileum and large intestine with subsequent systemic involvement. An abnormality of host response to infective agents, in general, was indicated by the unusually high occurrence of this disease, as well as other disease processes. Morphologic evaluation of lymphoid organs revealed decreased cellularity of follicles and decreased numbers of plasma cells in all macaques, whereas T cell-dependent areas varied from hypocellular to hypercellular with 5 macaques with malignant lymphoma. The spontaneous erythrocyte rosette-forming subpopulation of T cells was decreased in peripheral blood, but was increased in lymph nodes containing atypical mycobacterial lesions. Serum immunoglobulin value decreased progressively in diseased macaques. A basic abnormality of T-cell subpopulations controlling other components of host response was suspected. Macrophages from lesions that contain mycobacterial organisms did not phagocytize latex beads normally in vitro, whereas monocytes in the blood of the same macaques were capable of in vitro phagocytosis.
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PMID:Immunologic abnormality in a group of Macaca arctoides with high mortality due to atypical mycobacterial and other disease processes. 387 86

Birds were brooded reared, and laying house-tested at two widely separated sites: Animal Research Centre (ARC) and North Central Region Poultry Breeding Laboratory (NCRPBL). Two strain and a commercial stock were included only at NCRPBL. At ARC, all birds were brooded, reared, and laying house-tested in cages. At NCRPBL, half of the chicks were brooded and reared on floor and half in cages, and all hens were laying tested at one or two birds per cage. Most hens housed one per cage were tested for lymphoid leukosis virus (LLV) infection by the complement fixation test for group specific antigen in egg albumen. When all hens tested at NCRPBL were considered, the method of brooding and rearing affected only egg weight and body weight in favor of the hens reared in floor pens. The commercial stock and the strain crosses performed better than the control strains. Despite very similar genetic backgrounds, there were large differences between control strains 10 and NCR. Hens housed one per cage had lower mortality and higher egg production than those housed two per cage. Average performance of birds at ARC was somewhat better than that at NCRPBL, but there were genotype-site interactions for mortality, egg production, and sexual maturity. The frequency of shedders in the crosses (17.2%) was the same as that of the control strains (20.8%), but the frequency of shedders in the commercial stock (4.5%) was much lower. The method of brooding and rearing had no effect on the frequency of shedders. The LLV infection was associated with significant reductions in egg production and egg quality. For example, the difference between test-positive and test-negative hens was 25 eggs per hen housed and 16 eggs per surviving hen.
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PMID:The effects of geographical area, rearing method, caging density, and lymphoid leukosis infection on adult performance in egg stocks of chickens. 666 2

The Fas-Fas ligand (FasL) system plays an important role in the induction of lymphoid apoptosis and has been implicated in the suppression of immune responses. Herein, we report that gene transfer of FasL inhibits tumor cell growth in vivo. Although such inhibition is expected in Fas+ tumor cell lines, marked regression was unexpectedly observed after FasL gene transfer into the CT26 colon carcinoma that does not express Fas. Infection by an adenoviral vector encoding FasL rapidly eliminated tumor masses in the Fas+ Renca tumor by inducing cell death, whereas the elimination of Fas- CT26 cells was mediated by inflammatory cells. Analysis of human malignancies revealed Fas, but not FasL, expression in a majority of tumors and susceptibility to FasL in most Fas+ cell lines. These findings suggest that gene transfer of FasL generates apoptotic responses and induces potent inflammatory reactions that can be used to induce the regression of malignancies.
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PMID:Gene transfer of Fas ligand induces tumor regression in vivo. 939 Nov 18

The induction of tumor-specific T-cell responses that are effective in eradicating disseminated tumors and in mounting a persistent tumor-protective immunity is one of the major goals of tumor immunotherapy. Here, we demonstrate that we achieved this goal by directing interleukin 2 (IL-2) to the tumor microenvironment of colon carcinoma metastases in syngeneic mice with a recombinant antibody-IL-2 fusion protein (huKS1/4-IL-2). Eradication of established pulmonary metastases is induced by a CD8+ T cell-mediated immune response, which can be transmitted to naive syngeneic severe combined immunodeficient mice by adoptive transfer of CD8+ T cells from immune animals. This immune response was followed by the induction of a long-lived immunity against challenge up to 5 months later with CT26-KSA or wild-type CT26 murine colon carcinoma cells in BALB/c mice. This memory immune response was confirmed by flow cytometric analyses of CD8+ T cells isolated from secondary lymphoid tissue that revealed a phenotypic profile typical of early memory T cells. This long-lived protective tumor immunity was successfully boosted to become optimally effective in all experimental animals by injections of noncurative doses of IL-2 fusion protein 4 days after challenge with tumor cells. Taken together, our results indicate that the huKS1/4-IL-2 fusion protein elicits a long-lived cellular memory immune response that can be amplified by additional applications of IL-2 fusion proteins. This approach could become useful for the treatment of colorectal carcinoma in an adjuvant setting, particularly in patients with minimal residual disease.
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PMID:Induction of persistent tumor-protective immunity in mice cured of established colon carcinoma metastases. 973 3


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