UMLS:C0009443 - FACTA Search

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Query: UMLS:C0009443 (cold)
92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An in vitro model of antibody-dependent cellular cytotoxicity (ADCC) was established, using squamous-cell carcinoma of the head and neck (SCCHN) targets,human/mouse chimeric monoclonal antibodies (cMAbs) SF-25 and 323/A3 and human peripheral blood mononuclear cells (PBMC). We previously showed that natural killer (NK) cells are the main effector population mediating ADCC in the presence of the cMAbs. ADCC was significantly inhibited by the overnight pre-treatment of SCCHN targets with exogenous interferon-gamma (IFN-gamma). This inhibition was dose-dependent, reproducible and consistently observed with various SCCHN cell lines. SCCHN cells pre-treated with IFN-gamma had a significantly higher expression of intercellular adhesion molecule-I (ICAM-I) and major histocompatibility complex (MHC) class I antigens compared with untreated target cells. No differences in expression of the SCCHN-associated antigens on these targets or in the formation of NK-SCCHN conjugates were found, using flow cytometry. IFN-gamma-pre-treated SCCHN cells were less effective in competing with untreated targets in cold target inhibition assays and in inducing cytokine production from NK cells in co-incubation experiments. Protective effects of IFN-gamma on target cell sensitivity to lysis were blocked by pre-treatment of target cells with actinomycin-D or cycloheximide. The susceptibility of the target cells was restored by removal of MHC class I antigens from their surface by acid stripping before ADCC. Our results suggest that the decreased ADCC seen with SCCHN targets pre-treated with IFN-gamma is related to post-binding events, possibly altered signaling from targets to effector cells, and requires protein synthesis in the target cells.
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PMID:Protective effects of interferon-gamma on squamous-cell carcinoma of head and neck targets in antibody-dependent cellular cytotoxicity mediated by human natural killer cells. 862 Dec 63

gammadelta T cells can be grouped into discrete subsets based upon their expression of T cell receptor (TCR) variable (V) region families, their tissue distribution, and their specificity. Vdelta2+ T cells constitute the majority of gammadelta T cells in peripheral blood whereas Vdelta1+T cells reside preferentially in skin epithelium and in the intestine. gammadelta T cells are envisioned as first line host defense mechanisms capable of providing a source of immune effector T cells and immunomodulating cytokines such as interleukin (IL) 4 or interferon (IFN) gamma. We describe here the fine specificity of three distinct gammadelta+ tumor-infiltrating lymphocytes (TIL) obtained from patients with primary or metastatic colorectal cancer, that could be readily expanded in vitro in the presence of IL-1beta and IL-7. Irrespective of donor, these individual gammadelta T cells exhibited a similar pattern of reactivity defined by recognition of autologous and allogeneic colorectal cancer cells, renal cell cancer, pancreatic cancer, and a freshly isolated explant from human intestine as measured by cytolytic T cell responses and by IFN-gamma release. In contrast, tumors of alternate histologies were not lysed, including lung cancer, squamous cell cancer, as well as the natural/lymphocyte-activated killer cell-sensitive hematopoietic cell lines T2, C1R, or Daudi. The cell line K562 was only poorly lysed when compared with colorectal cancer targets. Target cell reactivity mediated by Vdelta1+ T cells was partially blocked with Abs directed against the TCR, the beta2 or beta7 integrin chains, or fibronectin receptor. Marker analysis using flow cytometry revealed that all three gammadelta T cell lines exhibit a similar phenotype. Analysis of the gammadelta TCR junctional suggested exclusive usage of the Vdelta1/Ddelta3/Jdelta1 TCR segments with extensive (< or = 29 bp) N/P region diversity. T cell recognition of target cells did not appear to be a major histocompatibility complex restricted or to be correlated with target cell expression of heat-shock proteins. Based on the ability of some epithelial tumors, including colorectal, pancreatic, and renal cell cancers to effectively cold target inhibit the lysis of colorectal cancer cell lines by these Vdelta1+ T cell lines, we suggest that intestinal Vdelta1+ T cell lines, we suggest that intestinal Vdelta1+ T cells are capable of recognizing cell surface Ag(s) shared by tumors of epithelial origin.
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PMID:Human intestinal Vdelta1+ lymphocytes recognize tumor cells of epithelial origin. 866 26

Following non-lethal heat stress (41.8 degrees C) and a recovery period at 37 degrees C, the inducible 72kDa HSP (HSP72) is detectable selectively on the cell surface of human Ewing's Sarcoma (ES) and of leukemic K562 cells but not on EBV transformed B cells (B-LCL) which were generated from PBL of healthy human volunteers. The HSP72 expression was measured by flowcytometric analysis using a monoclonal antibody (moAb) that specifically recognizes HSP72, the inducible form of the HSP70 group. The major histocompatibility complex (MHC) class I expression, detected with moAb W5/32 was not affected by non-lethal heat exposure and a recovery period at 37 degrees C for 12 h: ES cells express MHC class I molecules on about 80% of the cells; K562 cells exhibited no MHC class I expression neither before nor after heat shock. Inhibition of RNA-(actinomycin D) of protein-synthesis (cycloheximide) prior to heat treatment completely inhibits the expression of HSP72 on the cell surface of both tumour cells, thus indicating that de novo protein synthesis is required for HSP72 cell surface expression. Since, apart from HSP72, protein synthesis in general is down-modulated by heat shock we speculate that HSP72 molecules that are expressed on the cell surface of tumour cells might be recruited from newly synthesized proteins. The heat-inducible HSP72 cell surface expression on tumour cells could be correlated with an increased sensitivity of leukemic and sarcoma cells to lysis mediated by NK effector cells. The results of cold target inhibition assays revealed that histologically different tumour cells (sarcoma and leukemic cells) that were exposed to non-lethal temperatures have to share a similar if not identical HSP72 immunogenic determinant.
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PMID:Heat shock protein 72 (HSP72), a hyperthermia-inducible immunogenic determinant on leukemic K562 and Ewing's sarcoma cells. 902 25

Tissue concentrations of mercury were determined by cold vapor atomic absorption spectrometry in different inbred mouse strains after continuous treatment with HgCl2 (3 weekly sc injections of 0.5 mg/kg bw) for up to 12 weeks. Except for the thymus, in which steadily increasing mercury concentrations were found, in steady state levels of mercury were reached in blood and liver after 4 weeks and in spleen and kidney after 8 weeks. In the closely related strains C57BL/6, B10.D2, and B10.S, which differ only or primarily at the major histocompatibility complex, mercury concentrations in blood and liver were about twofold lower and renal concentrations were about three- to fivefold lower than those detected in strains A.SW and DBA/2. Another strain difference was observed in the spleen: after 8 and 12 weeks of continuous HgCl2 treatment, mercury concentrations in the spleen of strains A.SW, C57BL/6, and B10.S were significantly higher than those in strains DBA/2 and B10.D2. The strain difference in the spleen, an organ of the immune system, correlates with the susceptibility to the HgCl2-induced systemic autoimmune syndrome in mice in that the strains showing a higher mercury accumulation in the spleen are susceptible to this form of chemically induced autoimmunity, whereas the strains with lower mercury concentrations in the spleen are resistant.
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PMID:Strain differences in tissue concentrations of mercury in inbred mice treated with mercuric chloride. 916 80

Improving organ preservation techniques for transplantation is one of the most important goals of transplantation research. We have established a new, nonfreezing cryopreservation method to optimize the viability of rat kidneys for transplantation with up to 4 M dimethylsulphoxide (DMSO) in EuroCollins solution (EC) at -5 degrees C to -15 degrees C. We have confirmed the occurrence of a tubular and glomerular defect pattern that mediates acute tubular necrosis (ATN) and that may be a cause of major histocompatibility complex (MHC) independent immunological components of chronic transplant rejection. The extent of this defect [transplant survival and function, 31P-NMR spectroscopy, histological defect index] in the nonfreezing cryopreserved groups (n = 22) is significantly (P = 0.017) lower than in the simple cold storage group (n = 12). Quality and localization of the lesions in kidney transplants can elucidate the context of organ preservation, progressive hyperfiltration defects, and the occurrence of graft failure without elevated frequency of acute rejection episodes. These results indicate that further efforts to provide higher pretransplant organ viability without using it to prolong cold storage intervals may provide better insight into MHC-independent factors of chronic transplant failure and may result in improved long-term transplant outcome.
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PMID:Nonfreezing cryopreservation--a possible means of improving long-term transplant function? 956 79

Ex vivo exposure of malignant human T cells to photoactivated 8-methoxypsoralen (8-MOPa), followed by their i.v. return, appears to vaccinate patients against tumor-associated antigens of cutaneous T cell lymphoma in a procedure termed photopheresis. The molecular basis of this Food and Drug Administration-approved therapy, administered in 100 centers worldwide, is unclear. Most of the attention to the mechanism of action of the drug has focused on its capacity to form covalent cross-links with pyrimidine bases of DNA, thereby inhibiting cellular proliferation. Because immunologic factors appear to be important in the clinical response and could potentially serve as a model for immunotherapy of other malignancies, we explored the possibility that 8-MOP-treated cells display increased quantities of antigenic peptides at their cell surface. In this work, human B-lymphoblastoid tissue culture lines were exposed to 8-MOPa and expression of cell surface class I major histocompatibility complex proteins assessed, since CD8 T cells recognize antigenic moieties in the context of class I molecules. A peak 200-300% increase in MHC class I expression in 8-MOPa-treated cells occurred at 20 hr. 8-MOPa was far more effective in inducing this increase in class I MHC than other modalities, including mitomycin C, gamma-irradiation, ultraviolet B or heat or cold shock. This increase in surface class I MHC molecules appears to be driven by the degradation of cytoplasmic proteins into small peptides, followed by the transport of these peptides to MHC class I molecules in the endoplasmic reticulum. The data suggest that 8-MOPa treatment may augment the immunogenicity of tumor and/or antigen-presenting cells by enhancing processing and transport of class I MHC antigenic peptides.
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PMID:Photoactivated 8-methoxypsoralen treatment causes a peptide-dependent increase in antigen display by transformed lymphocytes. 972 96

Carcinoembryonic antigen (CEA), which is expressed in several cancer types, is a potential target for specific immunotherapy. HLA-A24 is the most frequent allele among Japanese and is also frequently present in Asians and Caucasians. We tested CEA-encoded HLA-A24 binding peptides for their capacity to elicit anti-tumor cytotoxic T lymphocytes (CTL) in vitro. For this purpose, we used CD8+ T lymphocytes from peripheral blood mononuclear cells (PBMC) of a healthy donor and autologous peptide-pulsed dendritic cells as antigen-presenting cells. This approach enabled us to identify 2 peptides, QYSWFVNGTF and TYACFVSNL, which were capable of eliciting CTL lines that lysed tumor cells expressing HLA-A24 and CEA. The cytotoxicity to tumor cells by the CTL lines was antigen-specific since it was inhibited by peptide-pulsed cold target cells as well as by anti-class I major histocompatibility complex (MHC) and anti-CD3 monoclonal antibodies (MAbs). The antigen specificity of the 2 CTL lines was examined using several tumor cell lines of various origins and for their peptide-dose responses. The identification of these novel CEA epitopes for CTL offers the opportunity to design and develop epitope-based immunotherapeutic approaches for treating HLA-A24+ patients with tumors that express CEA.
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PMID:Identification of HLA-A24 epitope peptides of carcinoembryonic antigen which induce tumor-reactive cytotoxic T lymphocyte. 993 37

In our previous study, using a swine model of single lung transplantation, a relationship between the level of major histocompatibility complex (MHC II) expression on host T lymphocytes and the extent of the ex vivo preservation time was observed. Furthermore, a model of ischaemia by simple cross-clamping proved MHC II up-regulation to be independent of tissue incompatibility. The mechanism through which ischaemia-reperfusion injury (IRI) induces MHC up-regulation in host peripheral T cells has not been reported. The objective of this study was to determine whether IRI induces MHC II up-regulation in T cells by altering the intracellular steady-state level of MHC II mRNA. Group A (seven donors, seven recipients) was an allotransplantation model of 15 h of cold storage (4 degrees C) while in group B (n = 6) animals underwent 2 h of warm ischaemia. Group C (n = 6) underwent sham operation. For quantification of mRNA extracted from peripheral T lymphocytes isolated before and after surgery, semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to determine the time at which mRNA levels reached its peak. The mRNA at pre-reperfusion and the time, at which mRNA peaked, was used for competitive RT-PCR. The results of RT-PCR analyses demonstrated that IRI induced an increase in the steady-state level of MHC II mRNA (p < 0.02) within 2 h post-reperfusion, irrespective of type of ischaemia and tissue incompatibility. In conclusion, this study suggested that IRI up-regulates the MHC II expression in peripheral T cells by altering the intracellular steady-state level of MHC II-DR-beta.
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PMID:The increase in the steady-state level of major histocompatibility complex mRNA in the host peripheral T lymphocytes due to ischaemia-reperfusion injury. 1054 41

The effects of cold stress (5 degrees C, 24 h) were investigated on the function and surface phenotype of peritoneal cells in the monocyte/macrophage lineage from young (8-10-week-old) and old (22-24-month-old) rats. The role of glucocorticoid (GC) in the immunomodulation by cold stress was also examined. The proportion of cells with a high density of ED2 (ED2high cells), expressing major histocompatibility complex (MHC) class II molecules, was significantly increased in peritoneal cells during cold stress in young, but not in old, rats. Antigen-presenting function was significantly higher in ED2high cells than in cells with a low density of ED2 (ED2low cells), thereby indicating that ED2high cells are at a functionally high level. While serum corticosterone concentration in old rats increased markedly after 3 h of cold stress, that in young rats did not vary substantially, and was followed by a significant decrease in both groups of rats after 24 h of cold stress. Administration of dexamethasone to young rats completely inhibited the increase of ED2high cells caused by cold stress. Meanwhile, the proportion of ED2high cells in young rats was significantly increased by adrenalectomy. Furthermore, nuclear translocation of a large amount of the GC receptor was observed in ED2low cells. These results suggest that cold stress enhances immune function in young rats, but not in old rats, and that the generation of ED2high cells are partly regulated by circulating GC level.
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PMID:Effects of ageing on generation of ED2high major histocompatibility complex class II+ macrophages during cold stress. 1063 74

The temporospatial relationship between microglial and astrocytic reactions and delayed thalamic cell death was examined 1-7 days following a traumatic cold lesion of the rat sensorimotor cortex using immunocytochemistry in combination with terminal deoxynucleotidyltransferase-mediated biotinylated dUTP nick end labeling (TUNEL) of nuclear DNA fragmentation. No or only occasional TUNEL-positive cells were found in the thalamic relay nuclei up to 3 days after trauma. After 7 days, on the other hand, a considerable number of TUNEL-positive cells were seen in the ventrobasal, the ventrolateral and posterior thalamic nuclei. Already 3 days after trauma, i.e., before cell injury was detectable, many protoplasmic astrocytes, which were reactive for glial fibrillary acidic protein, and ramified microglia, which were positive for complement receptor type 3b (CR3b) but negative for major histocompatibility complex (MHC) class II antigen, were noticed in the thalamus. The number of labeled astro- and microglia further increased after 7 days, when DNA fragmentation became evident. At this time, the morphology of microglia shifted towards bushy and rod-like cells, and microglia became also reactive for MHC class II antigen. Clusters of CR3b- and MHC class II-positive microglia were found in the ventrobasal thalamus. The present findings demonstrate that trauma-induced microglial and astrocytic reactions appear in the thalamus prior the onset of cell damage.
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PMID:Microglial and astrocytic reactions prior to onset of thalamic cell death after traumatic lesion of the rat sensorimotor cortex. 1067 21

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