Proceedings: Uptake and degradation of Ag and Ag Ab complexes by differently stimulated macrophages.
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Animals↗
Biomedical subjects
M Bar-Eli
Publications and source records attributed to M Bar-Eli.
Monocyte function in familial Mediterranean fever.
Monocytes derived from the peripheral blood of patients with familial Mediterranean fever (FMF) demonstrated a consistently lower phagocytic capacity (38-44%) for 125I-labelled Shigella flexneri when compared to monocytes from healthy subjects. Phagocytosis of both viable and killed Staphylococcus albus was similar in patients and controls. However, FMF monocytes had a two- to eight-fold depressed bactericidal capacity against S. albus in comparison to normal monocytes. Acid phosphatase and beta-glucuronidase monocyte activities were similar in patients and controls. It is suggested that the defects in monocyte function may be of importance in the pathogenesis of FMF. Colchicine had no effect on any of the indices studied.
Adolescent↗
Leukocyte chemotaxis in recurrent polyserositis (familial Mediterranean fever).
Polymorphonuclear leukocyte chemotaxis was investigated in 35 patients with recurrent polyserositis during attacks and during spontaneous or colchicine-induced remissions. Chemotaxis was found to be unchanged in the attack-free period in untreated patients, increased by about 50% during attacks, and decreased by about 50% during colchicine treatment.
Adolescent↗
Microtubules in PMNs from patients with familial Mediterranean fever.
Polymorphonuclear (PMN) cells derived from patients with Familial Mediterranean Fever (FMF) were evaluated in vitro for the function and concentration of their microtubules. Using the time-decay colchicine binding assay to determine the tubulin concentration in PMN cells, no difference was found in PMN cells derived from FMF patients in comparison with those from normal healthy subjects. Colchicine treatment had no effect on the detectable tubulin concentration in the cells. The mobility of fluorescent con A(F-con A)-receptor complexes on PMN membranes was used to test the function of the microtubules. PMNs from untreated FMF patients showed the same pattern of con A cap formation as seen in normal cells. PMNs derived from colchicine treated patients, however, showed 22-32% spontaneous cap formation. These cells also showed 10-30% more capping in comparison with normal or untreated FMF cells, for any given in vitro colchicine concentration, suggesting that at therapeutic doses, the colchicine does accumulate in the PMNs in vivo. We were unable to demonstrate a microtubule defect in the neutrophils from FMF patients in these studies.
Adolescent↗
NK sensitivity, H-2 expression and metastatic potential: analysis of H-2Dk gene transfected fibrosarcoma cells.
We have used the 3-Methylcholanthrene induced T-10 fibrosarcoma tumour cell system (H-2b xH-2k)F1 to elucidate the possible correlation between metastatic potential, expression of individual H-2 antigens and susceptibility to NK cells. Transfection of the non-metastatic and NK sensitive IC9 cells (Db+, Dk-, Kb-, Kk-) with the H-2Dk gene, altered the metastatic phenotype of the parental cells, yet had no effect on the susceptibility of these tumour cells to lysis by NK and did not elicit a specific CTL response in syngeneic hosts. Variants of the metastatic and NK resistant IE7 clone (Db+, Dk+, Kb-, Kk-), lacking H-2Dk, were selected by treatment with monoclonal anti H-2Dk antibodies and complement. These variants were sensitive to NK and poorly or non metastatic. Retransfection of 'Dk' 'loss' variants with the H-2Dk gene, resulted in the isolation of several clones expressing a wide range of metastatic phenotypes but maintained sensitivity to NK. These results indicate that the H-2D region of the MHC and or closely linked genes may be involved in the complex interrelationship between target susceptibility to NK and metastasis.
Animals↗
Intertumoral heterogeneity of receptor-tyrosine kinases expression in human melanoma cell lines with different metastatic capabilities.
Human melanocytes respond to several growth factors whose receptors have tyrosine kinase activity. Abnormalities in the expression of tyrosine kinase receptors may play an important role in the initiation and progression of melanoma. We therefore determined the steady-state mRNA expression of five tyrosine kinase receptors, epidermal growth factor receptor (EGF-R), c-met, nerve growth factor receptor (NGF-R), colony-stimulating factor receptor (CSF-R) and c-kit, in eleven human melanoma cell lines with different metastatic potentials in nude mice. All cell lines except for one nonmetastatic line established from a primary melanoma lost expression of c-kit. Expression of the other four tyrosine kinase receptors varied among the lines. The expression level of individual tyrosine kinase receptor did not correlate with the metastatic potential of the cells. These results suggest that metastatic human melanoma cell lines are heterogeneous for expression of tyrosine kinase receptors, with each cell type manifesting a distinct repertoire of receptor tyrosine kinases. The different profile of tyrosine kinase activities in different metastatic melanomas complicates its use for prognosis.
Animals↗
p53 gene mutation spectrum in human unknown primary tumors.
Mutations affecting the p53 gene are associated with many human malignancies, but little is known about changes in p53 in unknown primary tumors (UPTs), which are characterized as tumors with advanced stages of malignancy. We therefore investigated the frequency of p53 mutations in a series of 15 unknown primary tumor biopsies and eight cell lines established from UPTs. Mutations in the conserved regions of the p53 gene were verified by single-strand conformation polymorphism analysis of exons 5-9 and were verified by direct DNA sequencing of polymerase chain reaction products. A point mutation leading to an amino acid change in the p53 protein was found in six cases, and a mutation causing a change to termination was found in one case. A frameshift mutation was observed in one cell line. In one patient and one cell line we observed more than one mutation in the p53 coding sequence. Overall, the frequency of mutations that changed the p53 coding sequence in the UPTs we studied was 26% (6/23). Mutations were distributed in eight codons of the p53 gene. Seven of these tumors showed a reduction to homozygosity at the p53 allele, but one tumor apparently retained heterozygosity. We conclude that although UPTs represent highly metastatic advanced tumors that are expected to have a high incidence of p53 mutations, the frequency of p53 mutations is relatively low, suggesting that p53 mutations may not play a major role in the development and progression of this unique tumor type.
Amino Acid Sequence↗