Major histocompatibility complex class II expression on enterocytes: to present or not to present.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to G J Russell.
Explore the source record for details and available documents.
The binding of [3H]mebendazole ([3H]MBZ) to tubulin in benzimidazole-susceptible (BZ-S) and benzimidazole-resistant (BZ-R) strains of Trichostrongylus colubriformis and Caenorhabditis elegans was examined in order to investigate the biochemical changes to tubulin that result in BZ resistance in parasitic and free-living nematodes. In both species the extent of [3H]MBZ binding to tubulin was significantly reduced in the BZ-R strain compared with the BZ-S strain. The decrease in [3H]MBZ binding in the BZ-R strain of each species was the result of a significant reduction in the amount of charcoal stable [3H]MBZ-tubulin complexes and was not related to a change in the association constant of the [3H]MBZ-tubulin interaction. [3H]MBZ binding to tubulin was temperature dependent, reaching maximum levels at 37 degrees C in BZ-S T. colubriformis and 10 degrees C in BZ-R T. colubriformis. Both the BZ-S and BZ-R strains of C. elegans displayed maximum [3H]MBZ binding at 4 degrees C. Resistance ratios derived from the amount of [3H]MBZ binding in the BZ-S and BZ-R strains and in vitro development assays demonstrated that the temperature dependence and extent of drug binding was indicative of BZ resistance status and was species specific in the BZ-S isolates. These results indicate that biochemical differences exist in the binding of benzimidazole carbamates to tubulin in nematode species, and suggest that the susceptibility of the parasitic nematodes to the benzimidazole anthelmintics is the result of a unique high affinity and/or high capacity interaction of benzimidazole carbamates with tubulin.
Monoclonal antibodies to T-cell receptors were used to investigate the prevalence of the two distinct T-cell subpopulations (TCR alpha beta+ and TCR gamma delta+ cells) in the intestinal mucosa of children with celiac disease (gluten-sensitive enteropathy) as compared with normal intestinal mucosa. TCR gamma delta+ cells were rarely identified in the epithelium of human fetal or normal postnatal intestine and few were present in the lamina propria, whereas the number of distribution of TCR alpha beta+ cells closely resembled that of CD3+ cells. Compared with normal intestine, a significant increase in the number of CD3+, CD8+, TCR alpha beta+, and TCR gamma delta+ intraepithelial lymphocytes was present in celiac disease. Although the mucosal TCR gamma delta+ cells were less numerous than TCR alpha beta+ cells in celiac disease, there was a marked increase in the number of TCR gamma delta+ cells as compared with controls. The ligand recognized by the gamma delta T-cell receptor and the function of these cells have not been determined; however, these findings suggest a possible role for TCR gamma delta+ lymphocytes in mucosal immune responses and tissue injury as seen in celiac disease.
We describe a child with circulating anti-epithelial cell antibodies, autoimmune enteropathy with intestinal villous atrophy, and membranous glomerulonephritis. The patient had persistent diarrhea at 6 months of age, and a small bowel biopsy showed active enteritis, villous atrophy, and crypt hyperplasia. When the patient was, 10 months of age, nephrotic syndrome developed because of membranous glomerulonephritis. Results of tests for circulating immune complexes were negative. Indirect immunofluorescence studies revealed a circulating antibody directed against renal epithelial cells. Circulating antibodies directed against normal small intestine epithelial cells were also detected by the immunoperoxidase technique. Western blot and immunoprecipitation identified a 55-kd antigen, in both small bowel and kidney, that reacted with an antibody in the patient's serum. High-dose prednisone therapy induced a clinical remission, resolution of the small bowel injury, and diminished serum anti-epithelial cell antibodies; after dose reduction, clinical relapse occurred with villous atrophy and reappearance of anti-epithelial cell antibodies. When the patient was 45 months of age, persistent diarrhea recurred despite intravenous administration of corticosteroids, cyclosporine, and total parenteral nutrition. Autoantibodies to a 55-kd epithelial cell protein are temporally related to the development of enteropathy and nephropathy. Study of similar patients is needed to determine the role of such antibodies in this disorder.
Explore the source record for details and available documents.
STUDY OBJECTIVE: To examine the potential diagnostic value of the cardiac myofibrillar protein troponin-I as a target for radiolabelled antibodies in detecting heart damage, the uptake of 131I labelled polyclonal cardiac troponin-I Fab was investigated in necrotic myocardial cells in canine myocardial infarction. DESIGN: Cardiac specific troponin-I Fab was prepared by immunoaffinity chromatography and injected 5 h after coronary artery ligation. Whole body gamma camera scintigraphic images were taken after the injection, and heart slices were examined for the presence of labelled antibody. SUBJECTS: Adult dogs of either sex (n = 6) were used. MEASUREMENTS AND MAIN RESULTS: Scintigraphic whole body images at 24 and 40 h after troponin-I Fab injection showed increased 131I-localisation over the apical region of the heart which corresponded to the infarcted areas. Localisation in infarcted tissue was confirmed in isolated heart and histochemically stained heart slice images. Uptake of 131I Fab was up to 24 times greater in necrotic than in normal myocardium and was inversely related to regional blood flow as determined by 141cerium microsphere distribution. Confirmation that 131I Fab uptake was due to direct binding to troponin-I in necrotic cells was obtained by coinjection of non-immune 125I labelled Fab. CONCLUSIONS: Results indicate that troponin-I could act as a suitable target for detecting myocardial necrosis.
The development of the intestinal mucosal immune barrier is an important protective adaptation for postnatal life. The distribution and phenotype of T and B lymphocytes in human fetal intestine and lymphoid tissues have been characterized and compared to the distribution and phenotype of lymphocytes in postnatal intestine. The characterization of lymphocyte phenotype and MHC class II antigen distribution was done using MAb and an avidin-biotin complex immunohistochemical staining technique. Intraepithelial lymphocytes were occasionally present in fetal intestine and were primarily CD3+, CD8+. T lymphocytes were readily identified in the lamina propria of fetal intestine, but most were clustered in lymphoid aggregates. Cells identified by anti-IgA1 and anti-IgA2 were the most numerous cells of B cell lineage in the lamina propria of postnatal intestine, whereas IgM+ and IgD+ lymphocytes predominated in fetal tissues. However, IgA-bearing cells were identified in lymphoid aggregates of the intestine or spleen of some fetuses. This finding suggests that B lymphocytes can undergo Ig switching in utero. Additionally, fetal intestinal epithelial cells did not express MHC class II antigens, unlike some postnatal intestinal tissues. It is possible that postnatal events such as antigen exposure may be important for the induction of these class II antigens on intestinal epithelial cells.
The [3H]colchicine-binding activity of a crude supernatant of the free-living nematode Caenorhabditis elegans was resolved into a non-saturable component and a tubulin-specific component after partial purification of tubulin by polylysine affinity chromatography. The two fractions displayed opposing thermal dependencies of [3H]colchicine binding, with non-saturable binding increasing, and tubulin binding decreasing, at 4 degrees C. Binding of [3H]colchicine to C.elegans tubulin at 37 degrees C is a pseudo-first-order rate process with a long equilibration time. The affinity of C. elegans tubulin for [3H]colchicine is relatively low (Ka = 1.7 x 10(5) M(-1)) and is characteristic of the colchicine binding affinities observed for tubulins derived from parasitic nematodes. [3H]Colchicine binding to C. elegans tubulin was inhibited by unlabelled colchicine, podophyllotoxin and mebendazole, and was enhanced by vinblastine. The inhibition of [3H]colchicine binding by mebendazole was 10-fold greater for C. elegans tubulin than for ovine brain tubulin. The inhibition of [3H]colchicine binding to C. elegans tubulin by mebendazole is consistent with the recognised anthelmintic action of the benzimidazole carbamates. These data indicate that C. elegans is a useful model for examining the interactions between microtubule inhibitors and the colchicine binding site of nematode tubulin.
Twenty-five children with chronic constipation underwent serial monitoring of serum beta-carotene, retinol (vitamin A1), and alpha-tocopherol (vitamin E) levels during mineral oil therapy. Mineral oil was administered between meals. Patients were monitored for up to four months of therapy. Mean serum beta-carotene levels fell from 1.0 +/- 0.5 mumol/L (55.7 +/- 26.0 micrograms/dL) to 0.7 +/- 0.4 mumol/L (35.9 +/- 22.1 micrograms/dL) after the first month of mineral oil therapy and remained depressed throughout the remainder of the study. Serum alpha-tocopherol levels remained unchanged throughout the observation period. There was a modest increase in serum retinol levels during the study, especially after three months (from 1.48 +/- 0.84 mumol/L [42.3 +/- 24.1 micrograms/dL] to 2.22 +/- 0.77 mumol/L [63.5 +/- 22.1 micrograms/dL]). We conclude that while a short course of mineral oil can induce a reduction in the serum level of beta-carotene, the treatment has no adverse effect on serum levels of retinol and alpha-tocopherol.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A compilation of nucleic acid sequences from E. coli and its phages has been analysed for the frequency of occurrence of nearest neighbour base doublets and codons. Several statistically significant deviations from random are found in both doublet and codon frequencies. The deviations in E. coli also appear to occur in lambda and in the coat protein gene of MS2, whereas T4 and other parts of the MS2 genome show different sequence properties. These and other findings are discussed in relation to the hypothesis that rapidity of translation of mRNAs in the E. coli system is dependent on doublet frequency and codon usage patterns.
Explore the source record for details and available documents.
The buoyant densities of the DNA of herpes simplex virus type 1, type 2 and Pseudorabies virus, as determined in the analytical ultracentrifuge, are 1.725, 1.727 and 1.731 correlating with G+C contents of 67, 69 and 73 per cent respectively. The density differences for the DNA's of type 1 and type 2 herpes simplex viruses have been confirmed in experiments with isotopically labelled DNA from four type 1 and six type 2 strains by preparative CsCl gradient ultracentrifugation. The DNA of all the type 2 strains was denser than that of any of the type 1 strains examined. Despite these differences in DNA base composition of type 1 and type 2 strains, nearest neighbour analysis of their DNA's disclosed no obvious differences in doublet pattern or general design.
Explore the source record for details and available documents.
Explore the source record for details and available documents.