Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The patient is 11-year-old girl who was diagnosed as having hybrid acute leukemia (myeloid and lymphoid) from morphological (cytochemistry) findings, immunophenotype and genotype. During reinduction therapy after a second relapse, she presented hepatosplenomegaly and the remittent fever unresponsive to the intensified antibiotics. The diagnosis of reactive histiocytosis was made because of the remarkable elevation of serum ferritin value and proliferation of mature histiocytes in the bone marrow. Treatment with etoposide resulted in the disappearance of her fever and other symptoms. The subsequent refractoriness to platelet transfusion was also overcome by etoposide (p.o.) therapy. The results suggested that the treatment with etoposide might be effective for reactive histiocytosis and the related refractory state to platelet transfusion during therapy for leukemia.
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PMID:[Effectiveness of etoposide on reactive histiocytosis and refractory state to platelet transfusion during therapy of leukemia: case report]. 194 43

Iron-transferrin (FeTF) is an essential growth factor required for proliferation of lymphoid cells. FeTF activates protein kinase C (PKC) in the lymphoblastoid T-cell line, CCRF-CEM. We have treated CEM cells with human FeTF, then examined levels of PKC mRNA by hybridization analysis using cDNA probes specific for alpha-, beta-, and gamma-PKC subspecies. CEM cell mRNA hybridized with the beta-subspecies probe but not with probes for alpha- or gamma-subspecies. After exposure to FeTF an increase in PKC-beta mRNA was detectable at 10 minutes, peaked at 12 hours, and was sustained for 72 hours. Nuclear transcription assays demonstrated that rates of PKC-beta mRNA transcription were increased in FeTF-treated cells. By contrast, steady state levels of PKC-beta mRNA did not increase after treatment of cells with apotransferrin or gallium TF. Similarly, treatment with soluble iron as ferric ammonium citrate did not increase steady state levels of PKC-beta mRNA, despite producing a marked increase in cellular ferritin content. Ferritin increased from a baseline value of 63 ng/10(6) cells to 98 and 100 ng/10(6) cells in CEM cells treated for 1 hour with ferric ammonium citrate or FeTF, respectively. FeTF did not increase cytoplasmic-free calcium in CEM cells loaded with fura-2, indicating that binding of FeTF to transferrin receptors did not open membrane Ca2+ channels or release intracellular Ca2+. In addition, pretreatment of cells with desferrioxamine, but not ferrioxamine, blocked the FeTF-induced increase in PKC-beta transcripts. Therefore, iron as FeTF (not soluble iron or nonferric TF) stimulates transcription of the CEM cell PKC-beta gene. Transcriptional rate of the PKC-beta gene does not correlate with cellular iron content as judged by ferritin measurements. Furthermore, the requirement for FeTF does not appear to reflect activation of a classic agonist pathway as judged by stable cellular Ca2+. These data suggest that delivery of iron by FeTF to one or more specific cellular compartments may stimulate PKC-beta gene transcription in CEM cells.
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PMID:Induction of protein kinase C mRNA in cultured lymphoblastoid T cells by iron-transferrin but not by soluble iron. 200 52

Carbonic anhydrase cytochemistry of the ileal Peyer's patch in foetal and neonatal lambs has indicated secretion from the follicle-associated epithelium to the follicles. Reaction for carbonic anhydrase in the follicle-associated epithelium was found in the luminal plasma membrane, in cytoplasmic vesicles, and in vacuoles containing 50-nm membrane-bounded particles that seemed to be shed to the intercellular space. The lateral plasma membrane was negative for carbonic anhydrase, indicating that formation of carbonic anhydrase-positive particles was restricted to vacuoles. Administration of ferritin to ileal loops of sheep foetuses showed ferritin localized in vesicles and vacuoles of the follicle-associated epithelium followed by exocytosis, together with carbonic anhydrase-positive particles, into the indentations of the lateral cell border. The carbonic anhydrase-positive particles seemed to be transported to the centres of lymphoid follicles where many were attached to the plasma membrane of lymphocytes. Carbonic anhydrase-positive particles were also seen in vesicles and sometimes free in the cytoplasm of the lymphocytes or attached to their nuclear envelope. Light microscopically, carbonic anhydrase reactivity of the follicle-associated epithelium was associated with the early formation of the ileal Peyer's patch at about 100 days gestation. At this time the follicle-associated epithelium showed a strong luminal but at most a weak lateral staining. With further foetal development there was a progressive increase in the amount of carbonic anhydrase-positive reaction product in extracellular particles, both along the lateral cell borders of the follicle-associated epithelium and among the lymphocytes of the follicle centres.
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PMID:Transfer of carbonic anhydrase-positive particles from the follicle-associated epithelium to lymphocytes of Peyer's patches in foetal sheep and lambs. 211 54

Intravaginal immunization causes IgA responses in vaginal fluid, but so far lymphoid nodules in mouse vaginal mucosa have not been detected. The present study was therefore designed to test the hypothesis that IgA responses in the female reproductive tract may be generated in the regional iliac lymph nodes. Two, non-mucosal sites were identified in the female mouse pelvis, the subserous and presacral spaces, from which lymph drains mainly to the iliac nodes. Immunization at these pelvic sites with horse ferritin adsorbed to aluminum hydroxide (AH) caused much higher IgA and IgG titres in vaginal fluid than intravaginal immunization; moreover, the pelvic immunizations caused significantly higher and better sustained IgA titres in vaginal fluid than subcutaneous immunization near the scapulae or in the perineum, while IgG titres in vaginal fluid were similar in these groups. Additional mice were immunized with ferritin subcutaneously near the scapulae or in the presacral pelvic space using dimethyl dioctadecyl ammonium bromide (DDA), AH plus muramyl dipeptide, or the Ribi adjuvant system as adjuvants. Pelvic immunization caused higher IgA titres in vaginal fluid than subcutaneous immunization in each case. The IgA response stimulated by DDA was similar to that produced by AH but higher than the responses caused by the other two adjuvants, while IgG titres were similar with all four adjuvants in both sites. The results suggest that non-mucosal, pelvic immunization is particularly effective in stimulating IgA responses in the female reproductive tract. The observation is consistent with the possibility that the iliac lymph nodes may play a role in the development of IgA responses in the reproductive tract.
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PMID:Secretory immune responses in mouse vaginal fluid after pelvic, parenteral or vaginal immunization. 235 56

M cells of intestinal epithelia overlying lymphoid follicles endocytose luminal macromolecules and microorganisms and deliver them to underlying lymphoid tissue. The effect of luminal secretory IgA antibodies on adherence and transepithelial transport of antigens and microorganisms by M cells is unknown. We have studied the interaction of monoclonal IgA antibodies directed against specific enteric viruses, or the hapten trinitrophenyl (TNP), with M cells. To produce monospecific IgA antibodies against mouse mammary tumor virus (MMTV) and reovirus type 1, Peyer's patch cells from mucosally immunized mice were fused with myeloma cells, generating hybridomas that secreted virus-specific IgA antibodies in monomeric and polymeric forms. One of two anti-MMTV IgA antibodies specifically bound the viral surface glycoprotein gp52, and 3 of 10 antireovirus IgA antibodies immunoprecipitated sigma 3 and mu lc surface proteins. 35S-labeled IgA antibodies injected intravenously into rats were recovered in bile as higher molecular weight species, suggesting that secretory component had been added on passage through the liver. Radiolabeled or colloidal gold-conjugated mouse IgA was injected into mouse, rat, and rabbit intestinal loops containing Peyer's patches. Light microscopic autoradiography and EM showed that all IgA antibodies (antivirus or anti-TNP) bound to M cell luminal membranes and were transported in vesicles across M cells. IgA-gold binding was inhibited by excess unlabeled IgA, indicating that binding was specific. IgG-gold also adhered to M cells and excess unlabeled IgG inhibited IgA-gold binding; thus binding was not isotype-specific. Immune complexes consisting of monoclonal anti-TNP IgA and TNP-ferritin adhered selectively to M cell membranes, while TNP-ferritin alone did not. These results suggest that selective adherence of luminal antibody to M cells may facilitate delivery of virus-antibody complexes to mucosal lymphoid tissue, enhancing subsequent secretory immune responses or facilitating viral invasion.
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PMID:Binding and transepithelial transport of immunoglobulins by intestinal M cells: demonstration using monoclonal IgA antibodies against enteric viral proteins. 254 Nov 37

Monoclonal antibodies to the H and L subunits of ferritin were used in indirect immunofluorescent studies to investigate the subunit specificity of ferritin binding to transformed T and B lymphoid cell lines. Pre-incubation of cells with recombinant H ferritin followed by antibodies to the H subunit produced a labelling pattern in which all cells showed strong fluorescent stippling. Corresponding experiments with liver ferritin and an antibody to the L subunit revealed that most cells were lightly stippled, but 3-5% of the cells were intensely labelled. These two labelling patterns were distinct as assessed by cross-blocking experiments with recombinant H and liver ferritins. These results imply that different binding sites exist for each subunit.
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PMID:Identification of H- and L-ferritin subunit binding sites on human T and B lymphoid cells. 255 53

In 78 patients with myelofibrosis with myeloid metaplasia (MMM) the serum procollagen III peptide activity (s-PIIIP) had a higher mean value than in 22 normal adult volunteers (22.5 v. 10 ng/ml). Nevertheless, 21.8% of the patients had s-PIIIP within the 95th percentile of the normal control group (16 ng/ml): with respect to those whose concentrations exceeded this limit, patients with normal s-PIIIP levels were younger (55.8 v. 61.2 years), had a higher Hb value (12.3 v. 10.5 g/l), a lower serum ferritin level (106 v. 464 micrograms/l) and a higher platelet count (390 v. 216 x 10(9)/l). In the overall patient population, s-PIIIP was significantly higher in those with symptoms of active disease (fever, sweating, weight loss) than in subjects with non-active disease (28 v. 16.9 ng/ml). At univariate analysis s-PIIIP correlated (at the 5% level) with increasing WBC, serum ferritin and number of transfusions and with decreasing Hb and platelet count. At multivariate analysis increasing WBC, serum ferritin and age proved to be independently associated with s-PIIIP. No relationship was found between the s-PIIIP level and morphometric grading of bone marrow fibrosis, megakaryocyte number, or lymphoid infiltration. Longitudinal studies showed that s-PIIIP increased with disease progression. The conclusion of the study is that s-PIIIP correlates more with overall disease activity than with the extent of bone marrow fibrosis.
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PMID:Serum procollagen-III-peptide level correlates with disease activity in myelofibrosis with myeloid metaplasia. 273 39

The different amounts of H-rich and L-rich isoferritins found in malignant and non malignant lymphoid cells are accompanied by proportional variations in the relative quantity of messenger RNAs for the H and L subunits of ferritin. The correlation between levels of messenger RNAs and proteins suggests that the amount of messenger RNA plays an important role in ferritin biosynthesis in these cells. The enhanced expression of ferritin messenger RNAs in some neoplastic cells is not caused by gross alterations in the structure of ferritin genes.
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PMID:Regulation of ferritin synthesis in malignant and non-malignant lymphoid cells. 302 Nov 35

Members of the endogenous flora have become recognized as major pathogens in nosocomial infections, and the intestinal tract has become recognized as a major portal of entry for these pathogens. The English-language literature on this topic has been summarized and a working hypothesis devised describing a mechanism whereby intestinal bacteria can escape and cause systemic disease. It is postulated that the motile phagocyte ingests intestinal bacteria, transports them to extraintestinal sites, fails to accomplish intracellular killing, and then liberates the bacteria in the extraintestinal site. This hypothesis is consistent with many observations found in the literature: (1) The intestinal bacteria that most readily translocate out of the intestinal tract are classified as facultative intracellular pathogens. (2) Intestinal particles with no intrinsic motility (e.g., yeast, ferritin, starch) can translocate out of the intestinal lumen within hours after their ingestion. (3) The rate of translocation of intestinal bacteria can be altered with agents that modulate immune (including phagocytic) function. In the context of the mechanisms involved in intestinal immune responses, bacterial translocation appears to be a part of the normal antigen-sampling process of gut-associated lymphoid tissue. Systemic disease caused by translocating intestinal bacteria could be due to a maladaptation of the antigen-sampling process that has been designed to regulate the immune response to intestinal antigens.
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PMID:Proposed mechanisms for the translocation of intestinal bacteria. 305 94

Monoclonal antibody F30 was produced by the fusion of murine myeloma cell line P3-X63-Ag8-653 with spleen cells from a BALB/C mouse immunized with established human pancreatic cancer cell line (PK-1) and the reaction specificity was analyzed. The antigen recognized by monoclonal antibody F30 was different from HLA-associated antigen, beta 2-microglobulin, fetal bovine serum components, ferritin, AFP, or CEA. Monoclonal antibody F30 reacted with all of six pancreatic cancer cell lines established in our laboratory. Cross-reactivity was detected with a colon cancer cell line or an esophagus cancer cell line among various tumor cell lines tested. No reaction was detected with red blood cells, lymphocytes, or lymphoid and myeloid cell lines. By immunoperoxidase staining of frozen sections, the F30-defined antigen was detected not only on pancreatic cancer cell membrane but also on other adenocarcinomas. In addition, the monoclonal antibody F30 had a more wide-spread distribution on normal epithelial cells in the gastrointestinal organs, respiratory system, and urinary system. F30-defined antigen was composed of two protein components with molecular weight of 190 and 160 K. It was indicated that the antigen was an integral protein in the cell membrane since the antigen was not detected in the spent culture medium of antigen-positive cells.
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PMID:Human pancreatic cancer associated antigen detected by monoclonal antibody. 351 31


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