Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nonobese diabetic (NOD) mouse, in which major histocompatibility complex genes may be involved in the susceptibility to diabetes, has been developed as a model of autoimmune diabetes. The NOD mouse expresses I-A-encoded class II major histocompatibility complex antigens, which differ from those of other mouse haplotypes by the presence of a serine at position 57 of the A beta chain. Identifying islet autoantigens may help elucidate the role of class II antigens in the activation of autoreactive T cells and, thus, in the development of diabetes. We have detected autoantibodies directed against a 58-kDa islet cell antigen in NOD mice but not in other strains, including lupus-prone mice. Apart from insulin-secreting cells, the 58-kDa antigen was only found to be expressed by neuroblastoma cells and was identified as peripherin, an intermediate filament protein previously characterized in well-defined neuronal populations. This autoantigen cross-reacted with I-Anod class II antigens, suggesting that it may contribute to defective self-tolerance of islet beta cells in the NOD mouse.
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PMID:Peripherin: an islet antigen that is cross-reactive with nonobese diabetic mouse class II gene products. 172 86

A non-Fc receptor-bearing mouse neuroblastoma cell line, Neuro-2a, was used in indirect immunofluorescence tests to characterize the pattern of anti-neuronal activity of human sera in 41 cases of systemic lupus erythematosus (SLE), including seven cases of cerebral lupus, 30 "disease controls" (rheumatoid arthritis and chronic active hepatitis) and 30 healthy subjects. The immunofluorescence reaction with Neuro-2a gave a uniform ring fluorescence of the cell surface of cultured cells at 4 and at 37 degrees C, clusters were seen at 5 to 10 min and surface globules at 20 to 120 min. Titres of antibody to Neuro-2a in SLE ranged from less than 5 (seven cases), 5 to 20 (23 cases) and greater than or equal to 40 (11 cases). Titres of 80 to 160 were given by five of seven cases of cerebral lupus and two of 34 cases without cerebral lupus. Antibody to Neuro-2a was demonstrable in subjects without SLE, but to lower titres (less than 5-20). Of 11 SLE sera with antibody titres greater than or equal to 1:40, the antibody class was IgM in eight, IgG in two and both IgM and IgG in one. Absorption studies indicated that serum reactivity against Neuro-2a cells could be removed from some SLE sera with the cultured human neuroblastoma cell line, SK-N-SH, but not with mouse fibroblasts, mouse 3T3 cells, rat C6 glioma cells, rat transformed mesenchymal cells, nor by homogenates of mouse brain, heart, liver of kidney. Detection of antibody to Neuro-2a cell may be helpful in identifying patients with cerebral disease due to SLE.
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PMID:Autoantibody to a novel neuronal antigen in systemic lupus erythematosus and in normal human sera. 703 32

Hypoxia is known to induce extravasation of lymphocytes and leukocytes during ischemic injury and increase the metastatic potential of malignant lymphoid cells. We have recently identified a new adhesion molecule, hypoxia-activated ligand-1/13 (HAL-1/13), that mediates the hypoxia-induced increases in lymphocyte and neutrophil adhesion to endothelium and hypoxia-mediated invasion of endothelial cell monolayers by tumor cells. In this report, we used expression cloning to identify this molecule as the lupus antigen and DNA-dependent protein kinase-associated nuclear protein, Ku80. The HAL-1/13-Ku80 antigen is present on the surface of leukemic and solid tumor cell lines, including T and B lymphomas, myeloid leukemias, neuroblastoma, rhabdomyosarcoma, and breast carcinoma cells. Transfection and ectopic expression of HAL-1/13-Ku80 on (murine) NIH/3T3 fibroblasts confers the ability of these normally nonadhesive cells to bind to a variety of human lymphoid cell lines. This adhesion can be specifically blocked by HAL-1/13 or Ku80-neutralizing antibodies. Loss of expression variants of these transfectants simultaneously lost their adhesive properties toward human lymphoid cells. Hypoxic exposure of tumor cell lines resulted in upregulation of HAL-1/13-Ku80 expression at the cell surface, mediated by redistribution of the antigen from the nucleus. These studies indicate that the HAL-1/13-Ku80 molecule may mediate, in part, the hypoxia-induced adhesion of lymphocytes, leukocytes, and tumor cells.
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PMID:Hypoxia-activated ligand HAL-1/13 is lupus autoantigen Ku80 and mediates lymphoid cell adhesion in vitro. 1124 7