共查询到20条相似文献,搜索用时 15 毫秒
1.
Kalliopi P. Siziopikou Mi-Chung Ahn Larry Casey Mike Silver Jules E. Harris Donald P. Braun 《Cancer immunology, immunotherapy : CII》1997,45(1):29-36
It has been reported that the in vitro development of tumoricidal function in alveolar macrophages from lung cancer patients
is reduced significantly when compared to that in peripheral blood monocytes from the same patients or alveolar macrophages
from control patients. In the present investigation, a method for potentiating the development of tumoricidal function in
alveolar macrophages from lung cancer patients is described. This method, which relies on priming the macrophages with purified,
allogeneic peripheral blood lymphocytes from normal donors, could not be demonstrated when autologous lymphocytes from lung
cancer patients were used in the priming coculture. The augmentation of tumoricidal function appears to be mediated by one
or more soluble factors, since supernatants from cocultures of alveolar macrophages and allogeneic peripheral blood lymphocytes
could enhance the cytotoxic function of freshly obtained alveolar macrophages. Furthermore, it appears that NK cells are necessary
for this effect, since depletion of CD56+/CD57+ cells from allogeneic lymphocytes eliminated their capacity to enhance alveolar macrophage cytotoxic function. The augmentation
of cytotoxic function elicited in alveolar macrophages by this method was not associated with changes in the secretion of
tumor necrosis factor α, or interleukin 1β.
Received: 15 March 1997 / Accepted: 11 June 1997 相似文献
2.
To avoid destruction by complement, normal and malignant cells express membrane glycoproteins that restrict complement activity.
These include decay-accelerating factor (DAF, CD55), membrane cofactor protein (MCP, CD46) and protectin (CD59), which are
all expressed on colonic adenocarcinoma cells in situ. In this study we have characterised the C3/C5 convertase regulators
DAF and MCP on the human colonic adenocarcinoma cell line HT29. DAF was found to be a glycosyl-phosphatidylinositol-anchored
70-kDa glycoprotein. Blocking experiments with F(ab′)2 fragments of the anti-DAF monoclonal antibody BRIC 216 showed that DAF modulates the degree of C3 deposition and mediates
resistance to complement-mediated killing of the cells. The expression and function of DAF were enhanced by tumour necrosis
factor α (TNFα) and interleukin-1β (IL-1β). Cells incubated with interferon γ (IFNγ) did not alter their DAF expression. Two
MCP forms were expressed, with molecular masses of approximately 58 kDa and 68 kDa, the lower form predominating. MCP expression
was up-regulated by IL-1β, but not by TNFα or IFNγ. Expression of DAF and MCP promotes resistance of colonic adenocarcinoma
cells to complement-mediated damage, and represents a possible mechanism of tumour escape.
Received: 18 July 1995 / Accepted: 4 January 1996 相似文献
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4.
Paiotti AP Miszputen SJ Oshima CT Artigiani Neto R Ribeiro DA Franco M 《Journal of molecular histology》2011,42(5):443-450
Crohn′s disease (CD) is associated with gut barrier dysfunction. Tumour necrosis factor-α (TNF-α) plays an important role
into the pathogenesis of several inflammatory diseases because its expression is increased in inflamed mucosa of CD patients.
Anti-TNF therapy improves significantly mucosal inflammation. Thus, this study aimed to evaluate the effect of Etanercept
(ETC), a tumour necrosis factor alpha (TNF-α) antagonist on the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced experimental
colitis. A total of 18 Wistar rats were randomized into four groups, as follows: (1) Sham: sham induced-colitis; (2) TNBS:
non-treated induced-colitis; (3) ETC control; (4) ETC-treated induced-colitis. Rats from group 4 presented significant improvement
either of macroscopic or of histopathological damage in the distal colon. The gene expression of TNF-α mRNA, decreased significantly
in this group compared to the TNBS non-treated group. The treatment with etanercept attenuated the colonic damages and reduced
the inflammation caused by TNBS. Taken together, our results suggest that ETC attenuates intestinal colitis induced by TNBS
in Wistar rats by TNF-α downregulation. 相似文献
5.
Antibody-induced arthritis: disease mechanisms and genes involved at the effector phase of arthritis
During the development of rheumatoid arthritis (RA) autoantibodies to IgG-Fc, citrullinated proteins, collagen type II (CII),
glucose 6 phosphoisomerase (G6PI) and some other self-antigens appear. Of these, a pathogenic effect of the anti-CII and anti-G6PI
antibodies is well demonstrated using animal models. These new antibody mediated arthritis models have proven to be very useful
for studies involved in understanding the molecular pathways of the induction of arthritis in joints. Both the complement
and FcγR systems have been found to play essential roles. Neutrophils and macrophages are important inflammatory cells and
the secretion of tumour necrosis factor-α and IL-1β is pathogenic. The identification of the genetic polymorphisms predisposing
to arthritis is important for understanding the complexity of arthritis. Disease mechanisms and gene regions studied using
the two antibody-induced arthritis mouse models (collagen antibody-induced arthritis and serum transfer-induced arthritis)
are compared and discussed for their relevance in RA pathogenesis. 相似文献
6.
Panos Pantelidis Deirdre S McGrath Anne Marie Southcott Carol M Black Roland M du Bois 《Respiratory research》2001,2(6):365-8
Background
Previous studies have revealed that tumour necrosis factor (TNF)-α is upregulated in fibrosing alveolitis (FA) in humans. The aim of this study was to compare the TNF-α secretory profile of alveolar macrophages (AMs) and peripheral blood monocytes (Mos) of patients with cryptogenic FA and systemic sclerosis (SSc), a rheumatological disorder in which lung fibrosis can occur. In particular, we wished to assess whether TNF-α levels differ between SSc patients with FA (FASSc) and a nonfibrotic group. 相似文献7.
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9.
Xiangli Li Blair U Bradford Frederick Dalldorf Sanna M Goyert Stephen A Stimpson Ronald G Thurman Sergei S Makarov 《Arthritis research & therapy》2004,6(3):R273
Bacterial infections play an important role in the multifactorial etiology of rheumatoid arthritis. The arthropathic properties
of Gram-positive bacteria have been associated with peptidoglycan–polysaccharide complexes (PG-PS), which are major structural
components of bacterial cell walls. There is little agreement as to the identity of cellular receptors that mediate innate
immune responses to PG-PS. A glycosylphosphatidylinositol-linked cell surface protein, CD14, the lipopolysaccharide receptor,
has been proposed as a PG-PS receptor, but contradictory data have been reported. Here, we examined the inflammatory and pathogenic
responses to PG-PS in CD14 knockout mice in order to examine the role for CD14 in PG-PS-induced signaling. We found that PG-PS-induced
responses in vitro, including transient increase in intracellular calcium, activation of nuclear factor-κB, and secretion of the cytokines tumor
necrosis factor-α and interleukin-6, were all strongly inhibited in CD14 knockout macrophages. In vivo, the incidence and severity of PG-PS induced acute polyarthritis were significantly reduced in CD14 knockout mice as compared
with their wild-type counterparts. Consistent with these findings, CD14 knockout mice had significantly inhibited inflammatory
cell infiltration and synovial hyperplasia, and reduced expression of inflammatory cytokines in PG-PS arthritic joints. These
results support an essential role for CD14 in the innate immune responses to PG-PS and indicate an important role for CD14
in PG-PS induced arthropathy. 相似文献
10.
Johannes Grisar Philipp Hahn Susanne Brosch Meinrad Peterlik Josef S Smolen Peter Pietschmann 《Arthritis research & therapy》2001,3(2):127-10
In our study we characterised the immunophenotype of monocytes that migrated through an endothelial cell (EC) monolayer in vitro. We found that monocyte migration led to an enhanced expression of CD11a, CD33, CD45RO, CD54 [intercellular cell-adhesion molecule (ICAM)-1] and human leucocyte antigen-DR. The most striking increase was observed for ICAM-1 when ECs were activated with tumour necrosis factor-α and interleukin-1α. The results of our study indicate the following: (1) there is a characteristic immunophenotype on the surface of monocytes after transendothelial migration; (2) this phenotype seems to be induced by interactions between monocytes and ECs; and (3) this change is enhanced by the pretreatment of ECs with cytokines. Taken together, the results suggest that local cytokine production activating ECs is sufficient to enhance monocyte migration and that this, in turn, can induce changes consistent with an activated phenotype known to be interactive between antigen-presenting cells and T cells. These results have implications for our pathogenetic insights into rheumatoid arthritis. 相似文献
11.
Demir AY Groothuis PG Dunselman GA Schurgers L Evers JL de Goeij AF 《Cell and tissue research》2005,322(2):299-311
We have studied menstrual effluent in order to identify soluble menstrual factors that induce epithelial to mesenchymal transitions
(EMT) in mesothelial cells. A variety of molecules, such as nitric oxide and its reaction products, proteases (i.e. matrix
metalloproteinases, plasmin) and proteins and/or peptides (i.e. growth factors: b-fibroblast growth factor, epidermal growth
factor, hepatocyte growth factor, transforming growth factor-β; cytokines: interleukin 1β, tumour necrosis factor-α [TNF-α])
may be involved in this process. We have demonstrated that TNF-α is involved in EMT, whereas the other molecules are not.
Biochemical analysis has shown that the inducing menstrual factors are heat-labile molecules, are uncharged at neutral pH,
have a molecular weight between 50–70 kDa (or are bound in complexes of that size) and are eluted in the albumin fraction
during gel filtration chromatography. Further analysis of this fraction by using proteomics and mass spectrometry has led
to the identification of α-enolase and haemoglobin whose inhibition partially prevents EMT. When antibodies against TNF-α,
α-enolase and haemoglobin are combined, EMT is almost completely inhibited. Thus, the candidates for soluble menstrual factors
that induce mesothelial EMT are TNF-α, α-enolase and haemoglobin. 相似文献
12.
Yeo Dae Yoon Eun Sook Lee Jong Pil Park Mee Ree Kim Jun Won Lee Tae Hoon Kim Min Kyun Na Jin Hee Kim 《Biotechnology and Bioprocess Engineering》2011,16(6):1099-1105
Hizikia fusiforme is a commonly used food that possesses potent anti-bacterial, anti-fungal, and anti-inflammatory activities. The immunostimulatory
activities of aqueous extract of Hizikia fusiforme (HFAE) in RAW 264.7 macrophages and whole spleen cells were investigated. HFAE activated RAW 264.7 macrophages to produce
cytokines such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in
a dose-dependent manner. In addition, HFAE induced the mRNA expression of TNF-α, IL-1β, and IL-6 in RAW 264.7 macrophages.
Moreover, HFAE stimulated proliferation of whole spleen cells and reference mitogen. Taken together, the results demonstrate
that HFAE potently activates the immune function by regulating NO, TNF-α, IL-1β, and IL-6 in RAW 264.7 macrophage and promoting
spleen cell proliferation. 相似文献
13.
Several of the proinflammatory peptides involved in rheumatoid arthritis pathogenesis, including peptides induced downstream
of tumor necrosis factor-α as well as the monocyte/T cell-attracting chemokines RANTES and stromal cell-derived factor (SDF)-1α
and the neuropeptides vasoactive intestinal peptide (VIP) and substance P, have their biological half-lives controlled by
dipeptidyl peptidase IV (DPPIV). Proteolysis by DPPIV regulates not only the half-life but also receptor preference and downstream
signaling. In this article, we examine the role of DPPIV homologs, including CD26, the canonical DPPIV, and their substrates
in the pathogenesis of rheumatoid arthritis. The differing specific activities of the DPPIV family members and their differential
inhibitor response provide new insights into therapeutic design. 相似文献
14.
An S Hishikawa Y Liu J Koji T 《Apoptosis : an international journal on programmed cell death》2007,12(11):1989-2001
Although ischemia-reperfusion (I/R) of small intestine is known to induce lung cell apoptosis, there is little information
on intracellular and extracellular molecular mechanisms. Here, we investigated the mechanisms of apoptosis including the expression
of Fas, Fas ligand (FasL), Bid, Bax, Bcl-2, cytochrome c, and activated caspase-3 in the rat lung at various time-points (0–24 h)
of reperfusion after 1-h ischemia of small intestine. As assessed by TUNEL, the number of apoptotic epithelial cells, which
were subsequently identified as type II alveolar epithelial cells by electron microscopy and immunohistochemical double-staining,
increased at 3 h of reperfusion in the lung. However, intravenous injections of anti-TNF-α antibody decreased the number of
TUNEL-positive cells, indicating involvement of tumor necrosis factor-α (TNF-α) in the induction of lung cell apoptosis. Western
blotting and/or immunohistochemistry revealed a marked up-regulation of Fas, FasL, Bid, Bax, cytochrome c and activated caspase-3
and down-regulation of Bcl-2 in lung epithelial and stromal cells at 3 h of reperfusion. Our results indicate that I/R of
small intestine results in apoptosis of rat alveolar type II cells through a series of events including systemic TNF-α, activation
of two apoptotic signaling pathways and mitochondrial translocation of Bid. 相似文献
15.
The effect of feeding Lactobacillus fermentum I5007 on the immune system of weaned pigs with or without E. coli challenge was determined. Twenty-four weaned barrows (6.07 ± 0.63 kg BW) were randomly assigned to one of four treatments
(N = 6) in a factorial design experiment. The first two treatments consisted of healthy piglets with half of the pigs receiving
no treatment while the other half was orally administered with L. fermentum I5007 (108 CFU/ml) at a daily dose of 20 ml. Pigs in the second two treatments were challenged on the first day with 20 ml of E. coli K88ac (108 CFU/ml). Half of these pigs were not treated while the remaining pigs were treated with 20 ml of L. fermentum I5007 (108 CFU/ml). Peripheral blood lymphocytes subsets were determined using flow cytometry. The intestinal mucosal immunity of the
pigs was monitored by real time polymerase chain reaction. The cytokine content of the pig’s serum was also analyzed. Oral
administration of L. fermentum I5007 increased blood CD4+ lymphocyte subset percentage as well as tumor necrosis factor-α and interferon-γ expression in the ileum. Pigs challenged
with E. coli had elevated jejunal tumor necrosis factor-α while interferon-γ expression was increased throughout the small intestine.
There was no difference in the concentration of the cytokines interleukin-2, interleukin-6, tumor necrosis factor-α and interferon-γ
in the serum. CD8+ and CD4+/CD8+ in peripheral blood were not affected by treatment. In conclusion, L. fermentum I5007 can enhance T cell differentiation and induce ileum cytokine expression suggesting that this probiotic strain could
modulate immune function in piglets. 相似文献
16.
Summary The presence of immunoreactive pro-opiomelanocortin (POMC)-derived peptides (adrenocorticotropin hormone, β-endorphin, α-melanocyte-stimulating
hormone) and of cytokine-like molecules [interleukin (IL)-1α, IL-1β, IL-2, IL-6, tumour necrosis factor-α] was demonstrated
in periodic acid-Schiff-positive epithelial cells in the thymus of the goldfish (Carassius c. auratus) using immunocytochemical procedures. POMC-derived peptide- and cytokine-like molecules were localized in the same cell type.
Lymphocytes were negative for all the above mentioned molecules. Despite the smaller number of cells positive for neuropeptide-
and cytokine-like molecules, our findings suggest that immune-neuroendocrine interactions are likely to occur in the thymus
of goldfish. 相似文献
17.
Prediction of mutant activity and its application in molecular design of tumor necrosis factor-a 总被引:1,自引:0,他引:1
Two models for prediction of the activity and stability of site-directed mutagenesis on tumor necrosis factor-α are established.
The models are based on straightforward structural considerations, which do not require the elaboration of sitedirected mutagenesis
on the protein core and the hydrophobic surface area by analyzing the pmperties of the mutated amino acid residues. The reliabilities
of the models have been tested by analyzing the mutants of tumor necrosis factor-α (TNF-α) whose two leucine residues (L29,
L157) were mutated. Based on these models, a TNFα mutant with high activity was created by molecular design.
Project supported by the Chinese National High Technology Development Program. 相似文献
18.
Sergei Vyalov Alexis Desmoulière Giulio Gabbiani 《Virchows Archiv. B, Cell pathology including molecular pathology》1993,63(1):231-239
We have studied the formation of granulation tissue around osmotic minipumps delivering granulocyte macrophage-colony stimulating
factor (GM-CSF) chronologically in the rat using electron microscopy and immunohistochemistry at the light and electron microscopic
levels, with specific antibodies against α-smooth muscle (SM) actin and rat macrophages. At 2 and 3 days after pump implantation,
GM-CSF application produced an extensive inflammatory reaction characterized by edema and the accumulation of polymorphonuclear
cells and macrophages. Gradually, polymorphonuclear cells decreased in number and macrophages became arranged in large clusters.
The expression of α-SM actin in fibroblastic cells of the granulation tissue started from the 4th day after pump implantation
and progressed up to the 7th day. Double immunofluorescence staining showed macrophage clusters in relation to α-SM actinrich
fibroblastic cells. Electron microscopic examination confirmed that the fibroblasts containing α-SM actinpositive stress fibers
were found initially in close proximity to clustered macrophages. The delivery of plateletderived growth factor (PDGF) and
tumor necrosis factor-α (TNF-α) by the osmotic minipump induced an accumulation of macrophages, but in a much smaller number
compared with those seen after GM-CSF application; these macrophages were never assembled in clusters and, furthermore, TNF-α
and PDGF did not stimulate α-SM actin expression in fibroblastic cells. Our results suggest that after GM-CSF administration,
the cluster-like accumulation of macrophages plays an important role in stimulating α-SM actin expression in myofibroblasts.
Our results may be relevant to the understanding of the processes leading to granulation tissue formation in this and other
experimental models. 相似文献
19.
Tumor necrosis factor-α (TNF-α) is a polypeptide cytokine that has been associated with muscle wasting and weakness in inflammatory disease. Despite its potential importance in muscle pathology, the direct effects of TNF-α on skeletal muscle have remained undefined until recently. Studies of cultured muscle cells indicate that TNF-α disrupts the differentiation process and can promote catabolism in mature cells. The latter response appears to be mediated by reactive oxygen species and nuclear factor-κB which upregulate ubiquitin/proteasome activity. This commentary outlines our current understanding of TNF-α effects on skeletal muscle and the mechanism of TNF-α action. 相似文献
20.
Alveolar macrophages are indispensable for controlling influenza viruses in lungs of pigs 总被引:1,自引:0,他引:1
Kim HM Lee YW Lee KJ Kim HS Cho SW van Rooijen N Guan Y Seo SH 《Journal of virology》2008,82(9):4265-4274
Alveolar macrophages constitutively reside in the respiratory tracts of pigs and humans. An in vivo role of alveolar macrophages in defending against influenza viruses in mice infected with a reassorted influenza virus, 1918 HA/NA:Tx/91, was reported, but there has been no report on an in vivo role of alveolar macrophages in a natural host such as a pig using currently circulating human influenza virus. Here we show that in vivo depletion of alveolar macrophages in pigs by dichloromethylene diphosphonate (MDPCL2) treatment results in 40% mortality when pigs are infected with currently circulating human H1N1 influenza viruses, while none of the infected control pigs died. All infected pigs depleted of alveolar macrophages suffered from more severe respiratory signs than infected control pigs. Induction of tumor necrosis factor alpha in the infected pigs depleted of alveolar macrophages was significantly lower than that in the lungs of infected control pigs, and the induction of interleukin-10, an immunosuppressive cytokine, significantly increased in the lungs of infected pigs depleted of alveolar macrophages compared to infected control pigs. When we measured antibody titers and CD8(+) T lymphocytes expressing gamma interferon (IFN-gamma), lower antibody titers and a lower percentage of CD8(+) T lymphocytes expressing IFN-gamma were detectable in MDPCL2-treated infected pigs than in phosphate-buffered saline- and liposome-treated and infected pigs. Taken together, our findings suggest that alveolar macrophages are essential for controlling H1N1 influenza viruses in pigs. 相似文献