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)

A comprehensive immunologic and serologic analysis was performed on 31 untreated patients with Hodgkin's disease. Immune evaluations stressed T-cell functional activity and included traditional parameters (PHA responsiveness and delayed hypersensitivity skin reactivity), as well as newer functional assays (T-cell colony formation, chemotaxis, spontaneous and antibody-dependent cytotoxicity, and concanavalin A-induced suppressor cell activity (CISA). Serum factors included ferritin, prostaglandins, zinc, copper, immune complexes, and thymic hormone activity. Every patient exhibited at least one T-cell or serum abnormality. The greatest percentage of patients exhibited T-cell defects in chemotaxis (85%), colony formation (81%). and PHA reactivity (64%). Immune defects were more common with advanced disease but were not related to absolute T-cell or monocyte count, skin test anergy, or abnormalities of T mu/T gamma cell proportions. Linear relationships were identified among abnormalities in the three assays employing mononuclear cells (PHA, colony formation, CISA) which may have reflected the inhibitory influence of monocytes present in the mononuclear cell preparations. Low serum zinc correlated with marked impairment of T-cell chemotaxis. Elevated prostaglandins were associated with high PHA reactivity and with depressed colony formation. Our results indicate that many complex factors, including intrinsic T-cell defects, contribute to the impaired immunity associated with Hodgkin's disease.
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PMID:Multivariate analysis of T-cell functional defects and circulating serum factors in Hodgkin's disease. 645 60

The phenotypic features acquired subsequent to antigen-specific stimulation in vitro were evaluated by means of the kinetic expressions of CD69 and CD25 activation molecules on T lymphocytes and assayed by flow cytometry in response to PPD, Ag85B, and ferritin in PPD-positive healthy control individuals. In response to PHA, CD69 staining on both CD4+ and CD8+ T cells became initially marked after 4 h, peaked at 24 h, and quickly decreased after 120 h. For CD25, a latter expression was detected around 8 h, having increased after 96 h. As expected, the response rate to the mycobacterial antigens was much lower than that to the mitogen. Positive staining was high after 96 h for CD25 and after 24 h for CD69. CD69 expression was significantly enhanced (p < 0.05) on CD8+ as compared to CD4+ T cells. High levels were also found between 96-120 h. Regarding Ag85B, CD25+ cells were mostly CD4+ instead of CD8+ T cells. Moreover, in response to ferritin, a lower CD25 expression was noted. The present data will allow further characterization of the immune response to new mycobacterial-specific antigens and their evaluation for possible inclusion in developing new diagnostic techniques for tuberculosis as well in a new vaccine to prevent the disease.
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PMID:Kinetics of T cell-activation molecules in response to Mycobacterium tuberculosis antigens. 1256 72

Hereditary hemochromatosis (HH) is a common autosomal recessive disorder characterized by systemic iron overload with consequent tissue damage. The vast majority of HH patients are homozygous for the C282Y mutation in HFE, a non-classical MHC class-I gene located in chromosome 6, whose role in the regulation of systemic iron metabolism is still not completely understood. Iron enhances the formation of reactive oxygen species, with increasing risk of DNA damage induced by oxidative stress, and consequently an increased susceptibility to chromosome instability. In the present work we examined spontaneous and diepoxybutane (DEB)-induced chromosome instability in PHA-stimulated lymphocyte cultures from 23 HH patients, all homozygous for the C282Y HFE mutation, in comparison to 29 normal controls. In addition, three patients with secondary forms of iron overload, not related to HFE, were studied as controls to test the role of iron overload on DEB-induced chromosome instability. Our results show a significantly higher frequency of spontaneous chromosome breaks in lymphocytes from the HH patients, when compared with lymphocytes from normal controls (p<0.0001). In addition, there is a significant correlation between the percentage of cells with spontaneous chromosomal breaks and the transferrin saturation (r=0.53, p=0.0041) or serum-ferritin levels (r=0.66, p=0.0001) in patients. Surprisingly, the frequency of DEB-induced chromosome breaks was significantly lower in lymphocytes from HH patients than in lymphocytes from both controls and patients with secondary forms of hemochromatosis (p=0.0029). No correlation was observed between the percentage of cells with DEB-induced chromosome breaks and the transferrin saturation or serum-ferritin values. These results suggest that lymphocytes from HH patients may have an increased capacity to respond to DEB-induced chromosome breakage, and that this capacity is somehow related to the presence of the C282Y HFE mutation.
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PMID:Increased capacity of lymphocytes from hereditary hemochromatosis patients homozygous for the C282Y HFE mutation to respond to the genotoxic effect of diepoxybutane. 1914 86


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