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At least 163 records · Page 9Linked to original sources
PubMed1998

Nuclear antigen histone H1 is primarily involved in lupus erythematosus cell formation.

OBJECTIVE: To elucidate the nature of the antigen reactive with the "lupus erythematosus (LE) cell factor," the autoantibody involved in the LE cell phenomenon. METHODS: Serum samples from systemic lupus erythematosus (SLE) patients who were positive for the LE cell phenomenon (LEc+) and SLE patients who were negative for the LE cell phenomenon (LEc-) were used to characterize the nuclear antigen bound by the LE cell factor, by immunoblotting and immunoprecipitation techniques. RESULTS: All LEc+ sera, but none of the LEc- sera, uniformly reacted with a double band of MW approximately 30 kd in nuclear extracts. Depletion of nuclear protein extracts of antigens bound by pooled LEc- serum allowed precipitation of a low molecular weight protein by pooled LEc+ serum. This protein was able to block LE cell formation by LEc+ serum. Based on its reactivity with antihistone antibody and an electrophoretic mobility identical with that of precipitated and purified histone H1, this protein was identified as histone H1. Moreover, all LEc+ sera, but none of the LEc- sera, reacted with purified histone H1 by immunoblotting, whereas other histones were reactive with both types of sera. In addition, purified histone H1, but none of the other histones, strongly inhibited the induction of LE cells by LEc+ serum. CONCLUSION: Histone H1 represents the major antigenic component recognized by the LE cell factor. Thus, the LE cell phenomenon appears to be due primarily to anti-histone H1 reactivity.

Adult↗
PubMed1990

[Cytomorphologic concomitant reactions in malignant pleural effusions].

This study was undertaken to establish whether there might be certain cytological findings in the pleural effusions which, with a high degree of possibility, point to the presence of a malignant process despite the absence of tumour cells. In tumour cell-containing effusions we found LE cells in 26.5%, and psammoma bodies in 31.9% of the cases. In non-tumour cell-containing effusions with, nevertheless, malignant genesis, we detected LE cells in 12.5% and psammoma bodies in 0.8% of the cases. In three out of 6 rheumatogenic effusions, LE cells were also found. Otherwise, neither LE cells nor psammoma bodies were to be seen in any of the benign effusions (74 cases). Furthermore, in all the malignant pleural effusions, extremely atypical mesothelial cells were always detected, the identification and description of which proved difficult.

Diagnosis, Differential↗
PubMed1992

Mucin gel formed by tumorigenic squamous lung carcinoma cells has Le(a)-X oligosaccharides and excludes antibodies from underlying cells.

Cells of cloned lines of human squamous lung carcinomas elaborate large glycoproteins that are associated with their tumorigenic potential. Two groups of clones (called Le(a)-X-positive and Le(a)-X-negative) were studied that either do or do not express the Le(a)-X oligosaccharide associated with large glycoproteins and mucins secreted by these clones. Le(a)-X-positive cells elaborate a mucin gel complex associated with their apical surfaces, which appears as a mosaic of extracellular plates. Clones of this type are tumorigenic in nude rodents when injected s.c. or when introduced into the lungs via intrabronchial aerosol. By contrast, the Le(a)-X-negative clones do not form extracellular plates and are not tumorigenic in the lungs or subcutaneously. We demonstrate that the extracellular plates of Le(a)-X-positive cells exclude antibodies from interacting with the underlying squamous lung carcinoma cells and may therefore exert an immunoprotective effect. In support of this possibility it was found that: (a) There is a substantial inflammatory cell infiltrate associated with regressing nodules of Le(a)-X-negative cells in nude rodent lung and subcutaneous nodules, while there is no observable infiltration associated with progressing Le(a)-X-positive tumors. (b) In the brain (an immunoprivileged site) tumors develop and progress when either Le(a)-X-negative or -positive cells are introduced.

Animals↗
PubMed1978

[The lupus erythematosus (LE) phenomenon. Status in 1978].

The results of 835 studies of LE cells carried out over 8 years in 563 clinical cases of various nature are reported. The LE phenomenon--i.e. LE cells, LE globs and rosettes--was encountered exclusively in patients with LES, whereas tart-cells, nucleophagocytosis A and nucleophagocytosis B, although present in initial LES, and particularly in regressing LES, were very frequent in many other conditions. It is therefore held that true LE phenomenon is pathognomonic of LES since so-called AR with LE cells can be considered a clinical variant of LES, whereas lupoid hepatitis remains a vague, uncertain syndrome.

Arthritis, Rheumatoid↗
PubMed1992

Cytological aspects of pleural, peritoneal and pericardial fluids from patients with systemic lupus erythematosus.

Serous effusions of nine of 33 patients with systemic lupus erythematosus contained lupus erythematosus (LE) cells, identifiable in Papanicolaou-stained smears, wet films stained with toluidine blue, and cell blocks stained with haematoxylin and eosin. Specimens in which LE cells were found contained at least a moderate number of polymorphonuclear neutrophilic leucocytes. Most specimens containing LE cells also contained cells that resembled LE cells (tart cells), which appeared to be small macrophages that had phagocytosed a non-homogenized nucleus of a cell that had undergone degeneration. In 34 years of cytologic practice we have recognized LE cells in serous effusions only from patients who were already diagnosed as having systemic lupus erythematosus.

Adolescent↗
PubMed2006

Influence of IFN- alpha and IFN- gamma on lymphangiogenesis.

Malignant cancers commonly spread by local invasion followed by metastasis through venous or lymphatic passages or both to distant sites. Angiogenesis and its relation to tumor growth and metastasis have been extensively researched. To date, however, the role played by lymphangiogenesis and metastasis of cancer has been overlooked. Inhibition of lymphangiogenesis, compared with inhibition of angiogenesis, may provide new insight to the mechanisms of metastasis of cancers. The current study was designed to examine the effect of two commonly used inhibitors of angiogenesis, interferon-alpha (IFN-alpha ) and IFN-gamma, on the growth and proliferation of lymphatic endothelial (LE) cells isolated from pig thoracic duct under in vitro condition. The LE cells were isolated and marked using specific markers, such as VEGFR-3 and LYVE-1, before experimental studies. The results showed that treatment of LE cells derived from the thoracic duct with these two inhibitors caused a decrease in the rate of cell proliferation in a dose-dependent manner, as assessed by MTT assays (tetrazolium salt colorimetric assay). Cell migration rate was assessed by the speed at which the cell migrated out from the scrape-wound margin; the speed of migration of LE cells was significantly inhibited in a dose-dependent fashion compared with controls. Treatment with both IFN-alpha and IFN-gamma caused an increase in apoptosis of LE cells, as assessed by Hoechst staining and caspase-3 staining. Our results showed that both IFN-alpha and IFN-gamma were able to inhibit LE cell growth in a dose-dependent manner and that the inhibition may be through induction of apoptosis of endothelial cells.

Angiogenesis Inhibitors↗
PubMed1998

Response of lens epithelial cells to hydrogen peroxide stress and the protective effect of caloric restriction.

Hydrogen peroxide (H2O2) has been reported to be present at significant levels in the lens and aqueous humor in some cataract patients and suggested as a possible source of chronically inflicted damage to lens epithelial (LE) cells. We measured H2O2 effects on bovine and mouse LE cells and determined whether LE cells from old calorically restricted mice were more resistant to H2O2-induced cellular damage than those of same age ad libitum fed (AL) mice. Bovine lens epithelial cells were exposed to H2O2 at 40 or 400 microM for 2 h and then allowed to recover from the stress. The cells were assayed for DNA damage, DNA synthesis, cell viability, cell morphology, response to growth stimuli, and proliferation potential. Hydrogen peroxide-treated cells showed an increased DNA unwinding 50% greater than that for untreated controls. These DNA strand breaks appeared to be almost completely rejoined by 30 min following removal of the cells from a 2-h exposure. The 40 microM exposure did not produce a significantly lower DNA synthesis rate than the control, it responded to growth factor stimuli, and it replicated as did the control cells after removal of H2O2. The 400 microM H2O2 severely affected DNA synthesis and replication, as shown by increased cell size and by markedly reduced clonal cell growth. The cells did not respond to growth stimulation by serum or growth factors and lost irreversibly the capacity to proliferate. The responses of LE cells from old adlib diet (AL) and calorically restricted (CR) mice to H2O2 were significantly different. Exposure of LE cells to 20, 40, or 100 microM H2O2 for 1 h induces a significant loss of cellular proliferation in cells from old AL mice. LE cells from long-term CR mice of the same strain and age were more resistant to oxidative damage at all three concentrations of H2O2 than those of both old and young AL mice and showed a significantly higher proliferation potential following treatment. It is concluded that CR results in superior resistance to reactive oxygen radicals in the lens epithelium.

Age Factors↗
PubMed2005

Influence of angiostatin and thalidomide on lymphangiogenesis.

Malignant cancers commonly invade locally followed by spread through venous or lymphatic channels or both to distant sites. Hemangiogenesis and its relation to tumor growth and metastasis have been extensively studied. However, the role played by lymphangiogenesis in growth and metastasis of cancer has been largely neglected until just recently. Inhibition of lymphangiogenesis, as compared to inhibition of hemangiogenesis, may provide new insights into the mechanisms of cancer metastasis. The current study was designed to examine the in vitro effect of two commonly used inhibitors of hemangiogenesis, angiostatin and thalidomide, on the growth and proliferation of lymphatic endothelial cells isolated from pig thoracic ducts. We first isolated and characterized the lymphatic endothelial (LE) cells using specific markers for VEGFR3 and LYVE-1. The experimental results showed that treatment of the LE cells with these two drugs resulted in a decrease in the rate of cell proliferation in a dose-dependent manner as assessed by MTT assays. Cell migration rate was assessed by the speed of cell migration from the scrape-wound margin, and the results showed that migration of LE cells was also significantly inhibited in a dose-dependent fashion compared to controls. Treatment with angiostatin and thalidomide both resulted in an increase in apoptosis of LE cells as assessed by Hoechst staining and flow cytometry. We conclude that both angiostatin and thalidomide are able to inhibit LE cell growth in a dose-dependent manner and that the inhibition may be through induction of apoptosis.

Angiogenesis Inhibitors↗
PubMed1997

Mechanosensory neurons innervating Aplysia siphon encode noxious stimuli and display nociceptive sensitization.

Numerous studies of learning and memory in Aplysia have focused on primary mechanosensory neurons innervating the siphon and having their somata in the left E (LE) cluster of the abdominal ganglion. Although systematic analyses have been made of the responses of these LE cells to mechanical stimulation of the tightly pinned siphon, little is known about corresponding responses when the siphon is unrestrained. The present study demonstrates that LE mechanosensory thresholds in the freely moving siphon are much higher than in the pinned siphon. Light tactile stimuli adequate to activate central neurons and reflexive siphon movements often fail to activate the LE cells when the siphon is unrestrained. Because the LE cells display increasing discharge to increasing pressures, with maximal activation by crushing or tearing stimuli that cause tissue injury, they satisfy accepted definitions of nociceptor. Indeed, they show similarities to vertebrate Adelta nociceptors, including a property apparently unique (among primary afferents) to nociceptors-sensitization by noxious stimulation of their receptive field. Either pinching or pinning the siphon decreases LE cell mechanosensory threshold and enhances soma excitability. Such stimuli reduce effective tissue compliance and cause neuromodulation that enhances sensory responsiveness. These results, and recent descriptions of predatory attacks on Aplysia, suggest that LE sensory neurons are tuned to grasping and crushing stimuli that threaten or produce bodily harm. LE cell sensitization has effects, resembling hyperalgesia and allodynia, that compensate for loss of sensory function during injury and help protect against subsequent threats.

Afferent Pathways↗
PubMed1976

[Differential-diagnostic and prognostic significance of antinuclear factors].

On the patients of the consulting point for rheumatic diseases of the policlinical institute of the Karl-Marx-University Leipzig analytic examinations of the course for the existence of the LE-cell factor were carried out. We used the loose-body-test after van Soeren as screening test, controlled positive test results for several times under the same experimental conditions and supplemented it by the LE-cell test after Zinkham and Conley or later on by the immune fluorescence test. All patients with positive proof of LE-cells were examined for reference signs concerning a visceral lupus erythematodes, in which cases at the beginning of the examination nobody fulfilled the criteria of the diagnosis of a visceral lupus erythematodes. We tested the constancy of the proof of the LE-cells as well as the diagnosis in the course of longer periods. Typical changes of a visceral lupus erythematodes were seen only rarely. In 2 patients the joint processes were concomitant symptoms of a chronic aggressive hepatitis. In the p.c.p. at stage II to IV with positive LE-cell factors in the first place must be thought of a proof of LE-cell factors induced by drugs. In these cases gold is of practical importance. We could confirm that in contrast to the typical active visceral lupus erythematodes in p.c.p. the antinuclear factors have only a weakly positive result and are above all inconstant.

Antibodies, Antinuclear↗
PubMed1997

Long-term caloric restriction delays age-related decline in proliferation capacity of murine lens epithelial cells in vitro and in vivo.

PURPOSE: The goal of this study was to examine the effects of age and long-term caloric restriction on the proliferation capacity of murine lens epithelial (LE) cells in vitro and in vivo. METHODS: B6D2F1 (C57BL/6 X DBA/2) F1 mice 4 to 45 months of age were obtained and fed either an ad libitum (AL) or a calorically restricted (CR) diet (60% of AL intake). Cellular proliferation capacity in vitro was measured using the colony size distribution assay for 10-day clonal growth of mouse LE cells. Proliferation rate in vivo was assayed using immunostaining for 5-bromo-2'-deoxyuridine (BrdU) in mouse LE cells after 2-week osmotic pump delivery of BrdU. RESULTS: Proliferative capacity of cells from old AL mice decreased significantly in comparison to cells from young AL and old CR mice, as determined by the fractions of cells capable of forming small (no or one cell division) and large (four or more cell divisions) colonies in vitro. There was also a decline in cell replicative rate as measured by BrdU labeling index (LI) in vivo with increasing age in AL and CR mice. However, this decline was marked in AL mice between 10 and 30 months of age and minimal in CR mice. Significant differences in BudU LI between AL and CR mice occurred when animals were 30 months of age or older. This finding indicates that an age-related decline in cellular proliferation rate in vivo was delayed by CR. CONCLUSIONS: A significantly reduced proliferative capacity of LE cells is associated with increased age of mice and is delayed by long-term caloric restriction as measured in vitro and in vivo. How caloric restriction mediates its effects on LE cell proliferation remains to be investigated further.

Aging↗
PubMed2005

Drosophila Dok is required for embryonic dorsal closure.

Embryonic dorsal closure (DC) in Drosophila is a series of morphogenetic movements involving the bilateral dorsal movement of the epidermis (cell stretching) and dorsal suturing of the leading edge (LE) cells to enclose the viscera. The Syk family tyrosine kinase Shark plays a crucial role in this Jun amino-terminal kinase (JNK)-dependent process, where it acts upstream of JNK in LE cells. Using a yeast two-hybrid screen, the unique Drosophila homolog of the downstream of kinase (Dok) family, Ddok, was identified by its ability to bind Shark SH2 domains in a tyrosine phosphorylation-dependent fashion. In cultured S2 embryonic cells, Ddok tyrosine phosphorylation is Src dependent; Shark associates with Ddok and Ddok localizes at the cell cortex, together with a portion of the Shark protein. The embryonic expression pattern of Ddok resembles the expression pattern of Shark. Ddok loss-of-function mutant (Ddok(PG155)) germ-line clones possess DC defects, including the loss of JNK-dependent expression of dpp mRNA in LE cells, and decreased epidermal F-actin staining and LE actin cable formation. Epistatic analysis indicates that Ddok functions upstream of shark to activate JNK signaling during DC. Consistent with these observations, Ddok mutant embryos exhibit decreased levels of tyrosine phosphorylated Shark at the cell periphery of LE and epidermal cells. As there are six mammalian Dok family members that exhibit some functional redundancy, analysis of the regulation of DC by Ddok is expected to provide novel insights into the function of the Dok adapter proteins.

Amino Acid Sequence↗
PubMed1989

Lupus erythematosus cell formation by a monoclonal antibody derived from an autoimmune MRL/Mp-lpr/lpr mouse.

An MRP-2 monoclonal antibody (MoAb) was primarily a product of hybridoma selected by binding to poly(ADP-ribose) from a lupus prone MRL/Mp-lpr/lpr (MRL/l) mouse, and was shown to cross-react with single-stranded (ss) DNA. Detailed examination revealed that MRP-2 MoAb bound to a conformational epitope formed between double-stranded (ds) DNA and total histone: both H3 and H4 were essential for the formation of this conformational epitope with dsDNA. Because of this characteristic of the MoAb, its ability to induce lupus erythematosus (LE) cells was examined in an indirect LE test with peripheral blood of MRL/Mp-+/+ (MRL/n) mice, which develop a mild form of lupus after the age of one year. MRP-2 MoAb was found to induce hematoxylin bodies, LE rosettes and LE cells, but a direct LE test using MRL/n mouse blood did not induce LE cell phenomena. This is the first demonstration of induction of LE cells by a MoAb that binds to dsDNA-histone complexes.

Animals↗
PubMedDate not supplied

Lupus erythematosus cells in pleural fluid cytologic diagnosis in two patients.

Lupus erythematosus (LE) cells were demonstrated inpleural fluids from two patients with systemic lupus erythematosus (SLE). They were observed in preparations stained with the Giemsa and the Papanicolaou stains. The finding of LE cells in serous fluid has rarely been reported. Our results suggest that it is imporant to search for LE cells in serous fluid in patients in whom the diagnosis of SLE has not been established.

Adult↗
PubMed2005

Differential regulation of rodent hepatocyte and oval cell proliferation by interferon gamma.

Hepatocytes and intrahepatic progenitor cells (oval cells) have similar responses to most growth factors but rarely proliferate together. Oval cells constitute a reserve compartment that is activated when hepatocyte proliferation is inhibited. Interferon gamma (IFN-gamma) increases in liver injury that involves oval cell responses, but it is not upregulated during liver regeneration after partial hepatectomy. Based on these observations, we used well-characterized lines of hepatocytes (AML-12 cells) and oval cells (LE-6 cells) to investigate the potential mechanisms that regulate differential growth responses in hepatocytes and oval cells. We show that IFN-gamma blocks hepatocyte proliferation in vivo, and that in combination with either tumor necrosis factor (TNF) or lipopolysaccharide (LPS), it causes cell cycle arrest in hepatocytes but stimulates oval cell proliferation in cultured cells. The hepatocyte cell cycle arrest is reversible, is p53-independent, and is not associated with apoptosis. Treatment of AML-12 hepatocytes with IFN-gamma/LPS or IFN-gamma/TNF, but not with individual cytokines, induced NO synthase and generated NO, while similarly treated oval cells produced little if any NO. Generation of NO by an NO donor reproduced the inhibitory effect of the cytokine combinations on AML-12 cell replication, while NO inhibitors abolish the replication deficiency. In conclusion, we propose that IFN-gamma, in conjunction with TNF or LPS, can both inhibit hepatocyte proliferation through the generation of NO and stimulate oval cell replication. The response of hepatocytes and oval cells to cytokine combinations may contribute to the differential proliferation of these cells in hepatic growth processes.

Animals↗
PubMedDate not supplied

Correlation of serum interferon with some clinical and humoral signs of systemic lupus erythematosus.

The serum level of total interferon (IFN) was measured in 15 male patients with systemic lupus erythematosus (SLE) in the active phase and in remission, before and during corticotherapy. The values found were correlated with the clinical and humoral signs of disease. The IFN titer was high in the active phase of disease and was correlated with fever, extension of skin rash, polyarthritis, myositis, autoimmune hemolysis, cardiac and cerebral involvement as well as with ESR, reacting protein C, CIC, ANF and the percentage of LE cells. Isolated LE nephropathy without rapidly progressive or advanced renal failure was not associated with high IFN titer.

Adult↗
PubMed1990

Proliferation of omega 3 binding sites in the immune organs and leg infiltrate of rats with adjuvant induced arthritis.

The effects of chronic inflammatory lesions, induced by local injection of Freund's adjuvant into the rat hind limb, on omega 3 (peripheral type benzodiazepine) binding sites in the immune organs and leg infiltrate have been studied by autoradiography, using the specific photoaffinity ligand for omega 3 sites, 3H-PK 14105. In these arthritic rats, omega 3-site density in the thymus was about 2-fold greater than the values from control animals. Binding increases were similar in magnitude in the medulla and cortex. In contrast, omega 3 binding levels remained unchanged in the spleen. In the hyperplastic iliac lymph nodes, the morphological changes were accompanied by an increase in omega 3-site density in the proliferative centres and secondary follicles. In the inflammatory infiltrate of the leg an accumulation of omega 3-associated autoradiographic grains was observed over large multinucleated cells (possibly LE cells of Hargraves) and small thymocyte-like cells. Granulocyte-like cells located in the lumen of the vessels in the inflammatory lymph nodes and leg muscular infiltrate also had high amounts of autoradiographic grains. These findings demonstrate that in the inflammatory processes subsequent to the local injection of Freund's adjuvant, the activation of the immune system results in an increase in omega 3-site densities in immune organs and inflammatory lesions. This observation may be relevant to the proposed immunomodulatory role of these binding sites.

Affinity Labels↗