ABSTRACT
Dendritic cells (DCs) are antigen-presenting cells specialized to initiate and maintain immunity and tolerance. DCs initiate immune responses in a manner that depends on signals they receive from pathogens, surrounding cells and their products. Most tumors are infiltrated by DCs. Thus, interactions between DCs and dying tumor cells may determine the balance between immunity and tolerance to tumor cells. In addition, DCs also display non-immunologic effects on tumors and the tumor microenvironment. Therefore, improved understanding of the cross talk between tumor cells and DCs may suggest new approaches to improve cancer therapy.
Subject(s)
Cytokines/metabolism , Dendritic Cells/immunology , Dendritic Cells/physiology , Neoplasms/immunology , Neoplasms/physiopathology , Receptors, Cell Surface/metabolism , Toll-Like Receptors/metabolism , Animals , Cell Death , Cytokines/immunology , Humans , Immune Tolerance , Immunity, Cellular , Immunotherapy , Neoplasms/pathology , Neoplasms/therapy , Receptors, Cell Surface/immunology , Signal Transduction , T-Lymphocytes, Regulatory/immunology , Toll-Like Receptors/immunologyABSTRACT
Nr-CAM is a member of the immunoglobulin superfamily of neural cell-adhesion molecules initially thought to be expressed mainly in the brain. Here we show the presence of Nr-CAM protein in normal human pancreas and characterize its expression in hyperplastic and neoplastic human pancreatic tissue. Nr-CAM is expressed on the cell surface in normal pancreatic acini with enhanced staining at cell-cell junctions, and weak or no surface staining is seen on normal ductal cells. Nr-CAM expression is markedly up-regulated in intraductal hyperplasia. Expression was well maintained in well or moderately differentiated carcinoma but was reduced or absent from most poorly differentiated tumors. In addition, 4 of 4 human pancreatic adenocarcinoma cell lines tested demonstrated little or no Nr-CAM expression. This differential regulation of Nr-CAM expression suggests that it may be involved in the pathogenesis and invasive/metastatic behavior of pancreatic cancers. HUM PATHOL 32:396-400.
Subject(s)
Cell Adhesion Molecules/biosynthesis , Pancreas/metabolism , Pancreatic Neoplasms/metabolism , Biomarkers, Tumor , Gene Expression Regulation, Neoplastic , Humans , Hyperplasia , Pancreas/pathology , Pancreatic Neoplasms/pathologyABSTRACT
Recent data suggest that antibody-mediated suppression of erythroid progenitors may contribute to the anti-Kell-induced alloimmune hemolytic disease of the newborn (HDN). A 32-week-old girl who was positive for Kell was born to a mother who was negative for Kell but known to have anti-Kell antibodies. After birth, the baby had HDN and hyperbilirubinemia develop (peak bilirubin 21 mg/dL at day 9 of life). which was treated with phototherapy. Although the hyperbilirubinemia resolved, she became progressively anemic (hematocrit 22%) with an inappropriately low reticulocyte response (1.1%) and erythropoietin (EPO) level (20 mU/mL). To avoid the need for a blood transfusion, she was treated with recombinant erythropoietin (rEPO) and oral iron supplements. One week after starting EPO, the reticulocyte count increased to 9.1%. Erythropoietin therapy was continued for a total of 9 weeks, with resolution of her anemia at the end of therapy (hematocrit 35%). Thus, we were able to successfully treat the anemia with rEPO with avoidance of blood transfusion. This patient demonstrates that the antibody-mediated erythroid suppression in Kell alloimmune anemia can be overcome by rEPO. Recombinant erythropoietin should therefore be considered in the management of infants with severe or hypoproliferative anti-Kell-associated anemia.
Subject(s)
Autoantibodies/blood , Erythroblastosis, Fetal/immunology , Erythroblastosis, Fetal/therapy , Erythropoietin/therapeutic use , Kell Blood-Group System/immunology , Adult , Erythroblastosis, Fetal/blood , Female , Humans , Hyperbilirubinemia/drug therapy , Hyperbilirubinemia/therapy , Infant, Newborn , Infant, Premature , Phototherapy , Pregnancy , Recombinant ProteinsABSTRACT
In this article, we report a case of Leuconostoc bacteremia in a 7-month-old infant who had short-gut syndrome after a gastroschisis repair and who was dependent on total parenteral nutrition through a central venous catheter. The organism was initially misidentified as viridans group streptococcus. Detection of vancomycin resistance led to the correct diagnosis of Leuconostoc species. The patient was successfully treated with ampicillin and an aminoglycoside. A review of the literature revealed prematurity, short-gut syndrome, prior vancomycin use, and central venous catheters as important predisposing factors. Leuconostoc species is an emerging pathogen that should be considered in the differential diagnosis of vancomycin-resistant gram-positive bacteremia, particularly in these clinical settings.
