PDF superior Role of Leptin in the Activation of Immune Cells

Role of Leptin in the Activation of Immune Cells

Role of Leptin in the Activation of Immune Cells

On the other hand, leptin promotes T cell survival and Jurkat T lymphocytes survival [70] by modulating the expression of antiapoptotic proteins, such as Bcl-xL in stress- induced apoptosis [71]. This trophic effect of leptin on T cell is consistent with the reduction in lymphocyte numbers observed in fasted mice, that might be explained by the acute decrease in leptin levels [7, 19]. The role of leptin modulating T cell function in humans has been finally defined by clinical studies in specific and rare cases of patients with monogenic obesity. In human obesity due to congenital leptin deficiency, there is a T cell hyporesponsiveness (in addition to the expected neuroendocrine/metabolic dysfunction), and not only leptin treatment in these patients is an e ff ective lowering body weight but it can also revert T cell response to mitogen activation in vitro [72]. In addition, leptin has been necessary in nonagenarians ( ≥ 90 years old) to maintain functional naive CD8 T cells and a healthy immune system [73].
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8 Lee mas

New insights into the role of the immune microenvironment in breast carcinoma.

New insights into the role of the immune microenvironment in breast carcinoma.

Recently, immune edition has been recognized as a new hallmark of cancer. In this respect, some clinical trials in breast cancer have reported imppressive outcomes related to laboratory immune findings, especially in the neoadjuvant and metastatic setting. Infiltration by tumor infiltrating lymphocytes (TIL) and their subtypes, tumor-associated macrophages (TAM) and myeloid-derived suppressive cells (MDSC) seem bona fide prognostic and even predictive biomarkers, that will eventually be incorporated into diagnostic and therapeutic algorithms of breast cancer. In addition, the complex interaction of costimulatory and coinhibitory molecules on the immune synapse and the different signals that they may exert represent another exciting field to explore. In this review we try to summarize and elucidate these new concepts and knowledge from a translational perspective focusing on breast cancer, paying special attention to those aspects that might have more significance in clinical practice and could be useful to design successful therapeutic strategies in the future.
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11 Lee mas

The Alternative Epac/cAMP Pathway and the MAPK Pathway Mediate hCG Induction of Leptin in Placental Cells

The Alternative Epac/cAMP Pathway and the MAPK Pathway Mediate hCG Induction of Leptin in Placental Cells

upregulation as previously seen. As shown in Fig. 5D, similar results were observed in placental explants. These results suggest that activation of the cAMP/Epac alternative signaling pathway, and not the PKA pathway participates in hCG upregulation of leptin. To confirm the observed results, we performed transient transfection experiments with pL1951 plasmid. As shown in Figure 3. PKA blocks hCG stimulation of leptin. (A) BeWo cells were incubated during 3 days with hCG and/or H89, as indicated. Extracts from cells were prepared as previously described and loaded in a 12% SDS-PAGE. Leptin expression was determined by Western-blot. Loading controls were performed by immunoblotting the same membranes with anti-b-actin. Bands densitometry is shown in lower panels. Molecular weight (kDa) is indicated at the right of the blot. Representative results from three replicates are shown. (B) BeWo cells were transiently transfected with pL1951 and treated with 100 IU/ml hCG, 10 mM H89 and/or 100 mM SQ, or cotransfected with a plasmid expressing the catalytic subunit of PKA (PKA) (1 mg/ml) (C), or with a dominant negative mutant of the regulatory subunit of PKA (PKI) (1 mg/ml). Cells were incubated during 72 h in DMEM-F12 1% FBS media. Luciferase activity was measured in cellular extracts and normalized to b-galactosidase activity. Activity obtained with empty vector (PGL-3 basic vector) was set as a control. Results are expressed as mean 6 S.E.M. for three independent experiments. *p,0.05, **p,0.01, ***p,0.001 vs. control; #p,0.05, ###p,0.001 vs. hCG treatment.
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13 Lee mas

Role of Interleukin 10 in the modulation of the airway immune response during lung bacterial infection / |c Hernán F  Peñaloza Cerda ; thesis advisor Susan Bueno

Role of Interleukin 10 in the modulation of the airway immune response during lung bacterial infection / |c Hernán F Peñaloza Cerda ; thesis advisor Susan Bueno

Bacterial pneumonia is a major death cause worldwide, specially in children and the elderly. Two different types of pneumonia have been described: community acquired pneumonia and hospital associated pneumonia. Carbapenem-resistant Klebsiella pneumoniae ST258, an important agent of hospital acquired pneumonia may cause chronic infections with repeated episodes of bacteremia. In this thesis, we evaluated whether a clinical isolate of Carbapenem-resistant Klebsiella pneumoniae ST258 (KP35) is resistant to the clearance mediated by neutrophils and monocytes, which are the most important effectors cells against Klebsiella pneumoniae. During KP35 infection, there is an early recruitment to the lungs of Myeloid-derived suppressor cells (M-MDSCs). In this thesis we provide data that in vitro, BM-MDSCs infected with Klebsiella pneumoniae are highly efficient to suppress neutrophils bactericidal function. We next tested the hypothesis whether the early recruitment of these cells impairs KP35 clearance in vivo. Our data demonstrate early recruited M-MDSCs actively produce IL-10, which, contrary of what initially though, is important for KP35 clearance, reduction of lung damage, cytokine production and improvement of host survival. Bone marrow-derived MDSCs transfer from mice able to produce IL-10 to IL-10 -/- mice improved their ability to clear KP35 in the lungs
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269 Lee mas

UNDERSTANDING THE MOLECULAR MECHANISMS OF NETS AND THEIR ROLE IN ANTIVIRAL INNATE IMMUNITY

UNDERSTANDING THE MOLECULAR MECHANISMS OF NETS AND THEIR ROLE IN ANTIVIRAL INNATE IMMUNITY

Although the function of neutrophils has been widely described mainly in the context of bacterial infections, recently it was observed that neutrophils play essential roles in protection against viral infections or in enhancing viral replication or pathogenesis (Fig. 1). Some effector mechanisms of antiviral response by neu- trophils have been described in recent years, but further work is required to better understand the role of neutrophils in viral infections (Galani and Andreakos, 2015). The initial studies indi- cating that neutrophils arrive on the site of viral infection was reported for influenza A virus (IAV), which infects lungs and where neutrophil infiltration was virus dose-dependent (Bradley et al., 2012; Perrone et al., 2008; Short et al., 2014). Other viruses such as respiratory syncytial virus (RSV) can prolong survival of neu- trophils, in which are involved a phosphatidylinositol 3-kinase- (PI3K-) and nuclear factor-kappa B (NF- ␬ B) dependent pathway are involved (Lindemans et al., 2006). A high expression of impor- tant neutrophils attracting chemokines such as IL-8, Cxcl1 and CXCL2 to the RSV infection site has been reported. Although RSV has a limited capacity to replicate within neutrophils, an inter- action between neutrophils and RSV-infected fibroblasts has been demonstrated (Faden et al., 1984). For this reason, it has been sug- gested that direct activation of neutrophils by viral infection may not be the main phenomenon occurring in these infections; instead, these viruses may be infecting primarily the epithelium or may be activating immune cells, and the resulting immune response may initiate a robust neutrophil response (Tang et al., 2015). Further- more, in West Nile virus (WNV) infections, neutrophils were rapidly recruited to these sites (Bai et al., 2010; König et al., 1996; Perrone et al., 2008). In the case of Influenza virus infection, it was described that neutrophils were recruited specifically by the Influenza virus
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10 Lee mas

Levels of immune cells in transcendental meditation practitioners.

Levels of immune cells in transcendental meditation practitioners.

Our results would partly explain previous research supporting the effectiveness of TM practiced for preventing disease, lower medical utilization and expenditures, since NK cells play a role in tumor prevention and serve an early defense against intracellular infections. However, we cannot rule out that different levels in lymphocyte subset would have occurred due to external environmental factors. On the other hand, a small sample size is the major limitation of our paper. Further studies with a greater number of subjects are needed to confirm these findings.
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7 Lee mas

Leptin is an anti-apoptotic effector in placental cells involving p53 downregulation.

Leptin is an anti-apoptotic effector in placental cells involving p53 downregulation.

(unpublished results). They represent a valuable model for in vitro trophoblast studies. In this study we confirmed that leptin diminishes apoptosis in placental cells by virtue of the decrease of the Caspase-3 activation both in BeWo cells and in human placental explants. Moreover, when endogenous leptin expression was inhibited using an oligonucleotide complementary to leptin mRNA, cleaved Caspase-3 peptide increased. Leptin also dimin- ished the cleavage of PARP, a nuclear DNA-binding protein that Figure 5. Leptin reduces p53 levels in placenta. A) Swan-71 cells (16 10 6 cells) were plated in DMEM-F12 media in the absence of serum and incubated during 72 h with different leptin concentrations. Cell extracts were prepared as indicated in Materials and Methods and proteins were separated on SDS-PAGE gels. B) Placental explants were processed as described in Material and Methods and incubated in DMEM-F12 media supplemented with increasing leptin doses during 24 h. Placental extracts were prepared and proteins were separated on SDS-PAGE gels. In both cases (A and B) p53 was determined by Western blot analysis. DMEM-F12 10% FBS was used as a control. Molecular weights were estimated using standard protein markers. Molecular mass (kDa) is indicated at the right of the blot. Loading controls were performed by immunoblotting the same membranes with anti-a-GAPDH. Bands densitometry is shown in lower panels. Results are expressed as mean 6 SD for three independent experiments. C) p53 expression in human placental explants was determined by qRT-PCR. RNA was extracted as described in Materials and Methods. Statistical analyzes were performed by ANOVA. Asterisks indicate significant differences from the control according to Bonferroni’s multiple comparison post hoc test, relative to FBS 10% (#) or FBS 0% (*). # p,0.05, ## p,0.01, * p,0.05, ** p,0.01.
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12 Lee mas

Silica nanoparticles induce NLRP3 inflammasome activation in human primary immune cells

Silica nanoparticles induce NLRP3 inflammasome activation in human primary immune cells

activators and identified K + efflux as an event common among them all; however, mechanisms of ion channel opening related to NLRP3 activation remain unclear. 9 Several studies regarding immunological studies with NPs have been conducted using macrophage cell lines, but not in PBMCs or neutrophils; it was recently reported that macrophages differ in their mechanisms of inflammasome activation compared to other cells. The signals involved in inflammasome activation can be characterized as primers or activators of IL-1b pro- duction. The priming signals include PAMPs such as LPS and trigger the synthesis of inactive pro-IL-1b in macrophages via activation of TLRs, whereas elements such as K + efflux, ROS or lysosomal rupture are con- sidered upstream of inflammasome activation. While macrophages require two signals to produce mature IL-1b, monocytes and neutrophils constitutively express active caspase-1 and need only one signal for IL-1b release. 16,17 However, our study shows that in PBMCs, priming with LPS and then stimulating with SiNPs results in greater production of IL-1b than in non-primed cells.
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12 Lee mas

Assessment of allergen specific response in humans

Assessment of allergen specific response in humans

Current outbreak in allergic disease over recent years has coincided with progressive changes in our lifestyles (including hygiene, excessive antibiotic use and dietary change). The hygiene hypothesis, suggested that microbial exposure in early childhood is crucial for normal development of the immune system [Strachan, 1989]. This hypothesis was revised by Wold in 1998. He proposed that lack of early colonization of microbiota in the gut has the potential to influence the risk of allergic disease [Wold, 1998]. A mutualistic relationship between microbes and the immune system has played a critical role in normal immune development and regulation [West, et al., 2014]. Lack of regulatory responses may promote chronic inflammatory disease. Immune dysregulation has been clearly related to the failure in the colonization of microbes in the GALT of mouse models [Sudo, et al., 1997]. Recent reports showed that infant microbiomes have lower species richness than adults. Indeed, recent studies have shown lower abundance of Bacteroides and Clostridium in infants with food allergy [Tsuji, et al., 2012] [Penders, et al., 2013] [Azad, et al., 2013] [Jakobsson, et al., 2014] [Yang, et al., 2014]. Interestingly, it has been reported that sensitization to a food allergen is increased in mice that have been treated with antibiotics or are devoid of commensal microbiota [Stefka, et al., 2014]. Furthermore, IL-17 production was abolished in mice that were treated with large-spectrum antibiotics, suggesting that their differentiation depends on foreign antigens provided by the gut microflora [Lemaire, et al., 2011]. T H 17 cells have critical roles in
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227 Lee mas

TítuloNitric oxide mediated cortical activation: a diffuse
wake up system

TítuloNitric oxide mediated cortical activation: a diffuse wake up system

project locally. In their projection to the cortex, some authors suggest that cells may project over wide areas, whereas others suggest more restricted terminations (Zaborszky et al., 1999; Semba, 2000), which may in fact reflect multiple roles for the various components of this heterogeneous structure. Acetylcholine has been implicated in the transition from sleep to wake, but recently, an active role in the promotion and maintenance of sleep has also been proposed, as well as involvement in attention, motivation, and learning (for review, see Zaborszky et al., 1999; Semba, 2000; Sarter and Bruno, 2000). Despite this near-exponential expansion in proposed functions, one facet has remained relatively unchanged: the role of the BF in arousal, mediated via ACh release within the cortex, enhancing cell responsiveness and increasing signal-to-noise ratios, shifting the cortex from the classical sleep slow-wave EEG pattern to the desyn- chronized waveform of wake and arousal. The high concentration of cholinergic cells of the Ch4 group at the caudal end of the structure makes this the logical target for the experimental paradigms we have reported above. As expected, electrical stimulation of this region resulted in a shift in recorded EEG, or ECoG, from slow-wave activ- ity to desynchronous, higher frequency, low-amplitude spectra, as shown, for example, in Figure 2. Interestingly, our electrical stimu- lation paradigm induced such changes in widespread cortical re- gions (S1 and V1, simultaneously). However, we should not suggest too much about the nonspecificity exhibited (our stimulation pa- rameters were chosen to maximize activation to test a simple hy- pothesis); i.e., that some component of this arousal was mediated by the gaseous neurotransmitter NO.
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9 Lee mas

Th1 and Th17 hypercytokinemia as early host response signature in severe pandemic influenza.

Th1 and Th17 hypercytokinemia as early host response signature in severe pandemic influenza.

significantly higher levels of IL-17 and TNF-α in severe non critical patients compared to mild (difference not found for crit- ical ones), could reflect a beneficial role of these cytokines in this particular subset of patients. The patient who died five days after disease onset showed high viral load and undetec- table IL-17 levels in serum. This could reflect a protective role of IL-17 in severe patients. IL-15, IL-12p70, IL-6 constituted a hallmark of critical illness in our study. These three cytokines also mediate both antiviral and pro-inflammatory responses. IL- 6 is a potent regulator switching immune responses from the induction of Foxp3+ regulatory T cells to pathogenic Th17 cells in vivo [33]. IL-15 promotes CD8 T cells homeostatic proliferation [34] in response to infection. IL-12 plays a key role in the switch from innate to adaptive immunity [17]. Figure 2
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11 Lee mas

A Multifaceted Analysis of Immune Endocrine Metabolic Alterations in Patients with Pulmonary Tuberculosis

A Multifaceted Analysis of Immune Endocrine Metabolic Alterations in Patients with Pulmonary Tuberculosis

Very recently, Kim at al. [20] reported no differences in leptin and ghrelin levels in TB patients, although further separation into well-nourished or malnourished cases revealed lower amounts of ghrelin in the latter subgroup. Reasons for differences between this and our study findings may be of different nature. Our sample population was composed of untreated patients whereas in the Korean study patients were bled within 3 days following treatment initiation. Additional factors, i.e, genetic and environmental or predisposing factors may be also implied. In distinguishing prior malnutrition from the consumption state that accompanies progressive disease, the preserved nutritional status of close HHC of present TB patients adds support to the latter possibility. Whatever the case, it may be assumed that anorexia and the consumption state during TB are the result of a complex network of mediators with additive, interactive, and antagonistic interac- tions, in a not necessarily unique scenario. A candidate to play a role in these interactions is IL-6. As seen in a former study [12], IL-6 levels are increased in TB patients and this cytokine is known to reduce retroperitoneal fat and circulating levels of leptin [31]. Our results are also in line with the findings from Stenlof et al. [32] reporting a negative correlation between IL-6 levels in cerebral- spinal fluid, body weight and serum leptin concentrations in obese patients. Another factor likely involved in the catabolic state may be IL-1b. This cytokine was not only increased during TB but also negatively correlated with the BMI. At the experimental level IL- 1b is known to produce a profound hypoglycemia in mice and a re-setting of glucose homeostasis that favors fuel re-distribution towards immune cells but with a paradoxical reduction of food intake [33]. Moreover leptin actions on food intake and body temperature appear to be mediated by IL-1 [34].
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8 Lee mas

Role of oleic acid in immune system; mechanism of action; a review

Role of oleic acid in immune system; mechanism of action; a review

Membrane phospholipids are involved in the signal transduction pathways started out of the cell. Dietary unsaturated fatty acids or cells treatment with fatty acids, leads to their esterification in sn-2 position of membrane phospholipids. Once incorporated in the phospholipids, they can be hydrolyzed by several phospholipases. Phospholipases A 1 and A 2 (PLA 1 and PLA 2 ) lead to the release of those fatty acids present in sn-1 and sn-2 position of the glycerol, respectively, and to the subsequent lysophospholipides generation. Phospholipase C (PLC) hydrolyzes PIP 2 releasing also two second messengers: DAG and IP 3 . Phospholipase D (PLD) acts mainly on phosphatidilcoline (PC) and leads to the production of phosphatidic acid (PA), which is rapidly hydrolyzed to form DAG. Additio- nally, PA can also activate PLC and increase the affi- nity of the enzyme for the subtract. 86,87 As PA is the
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13 Lee mas

Ubiquitylation of the chemokine receptor CCR7 enables efficient receptor recycling and cell migration

Ubiquitylation of the chemokine receptor CCR7 enables efficient receptor recycling and cell migration

Chemokine receptors represent a family of seven-transmembrane spanning, G-protein-coupled receptors which interact with chemotactic cytokines termed chemokines. Chemokine receptor triggering results in the onset of complex intracellular signaling cascades leading to cell polarization and migration towards the chemokine source (Thelen and Stein, 2008). Cell migration is pivotal for the induction of immune responses and hence is tightly regulated (Bromley et al., 2008). The chemokine receptor CCR7 is mainly expressed on naı¨ve lymphocytes and mature dendritic cells and responsible for the homing of these cells to secondary lymphoid organs where dendritic cells present the acquired antigens to T cells (Fo¨rster et al., 2008). CCR7 has two known ligands, CCL19 and CCL21, which are both constitutively expressed by stroma cells in lymphoid tissues (Luther et al., 2000). Stimulation of CCR7 with either ligand was shown to similarly induce cell migration of primary T cells (Bardi et al., 2001; Schaeuble et al., 2011) and 300-19 transfectants (Otero et al., 2006; Willimann et al., 1998), G protein activation in H9 T cells (Kohout et al., 2004), ERK-1/2 phosphorylation in HEK293 transfectants (Kohout et al., 2004), and calcium mobilisation in primary T cells as well as various T cell lines (CEM, HuT78, H9) and HEK293 or 300-19 transfectants (Bardi et al., 2001; Kohout et al., 2004; Otero et al., 2008; Otero et al., 2006). In contrast, only CCL19 triggering resulted in CCR7 phosphorylation on serine/ threonine residues in HEK293 transfectants (Kohout et al., 2004) and b-arrestin2 binding (Byers et al., 2008; Comerford et al., 2006;
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12 Lee mas

A chronic pain: inflammation dependent chemoreceptor adaptation in rat carotid body

A chronic pain: inflammation dependent chemoreceptor adaptation in rat carotid body

chemoattractant chemokine, MCP-1 was further elevated beyond 6-fold after 3 days, and it remained at a similar level on day 7. CH induced a more gradual increase in IL-6 which was measured at ~3-fold and ~2-fold following 3 and 7 days of CH, respectively. Interestingly, following 28 days of hypoxia the expression of inflammatory molecules was normal, with the exception of IL-6 which was some 5.5-fold above normal, suggesting that this latter cytokine may play a maintenance role in chemoreceptor adaptation. Support for the validity of the qPCR assays was provided by assessments of the mRNA transcript level of tyrosine hydroxylase (TH), which is known to increase in type I cells during CH (figure 2). Additional studies in our laboratory showed that cytokine production was not limited to immune cells (Liu et al. 2009). Indeed, in situ hybridization experiments showed that IL-6 expression during CH is increased to high levels in putative type II cells, while a smaller but substantial elevation in probe signal was localized to cell clusters displaying morphology consistent with type I cells. We also used amplified RNA (aRNA) technology to
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18 Lee mas

Role of leptin in female reproduction.

Role of leptin in female reproduction.

Reproductive function, as other physiological functions, depends on the energy reserves stored as fat in adipose tissue. The large energy requirement of a hypothetical pregnancy in the future was the original rationale for explaining the disruption of reproductive function by low fat stores in the present. The teleological nature of this argument compelled investigators to search for an endo- crine signal that conveys information to the brain about the size of fat stores [1]. In 1994, leptin was the first adi- pokine claimed to be the ‘missing link’ between fat and reproduction. Leptin is a 16 kDa peptide hormone secreted mainly from adipose tissue which plays an integral role in the regulation of body weight and energy expenditure [2]. Plasma levels of leptin are correlated with the degree of obesity and are regulated by feeding and fasting. At present, leptin is considered to be a multifunctional hormone that regulates not only body weight homeosta- sis, but also thermogenesis, angiogenesis, hematopoie- sis, osteogenesis, chondrogenesis, neuroendocrine, and immune functions, as well as arterial pressure control [3–6]. These actions of leptin are consistent with its production by various tissues and organs, such as the stomach, skeletal muscle, pituitary cells and the placenta [7]. Compelling evidence has also implicated leptin in reproductive functions, such as the regulation of ovarian function, oocyte maturation, embryo development as well as implantation and placentation [8, 9]. This influence of leptin on human reproductive function was indicated by observed associations of leptin or leptin-receptor defi- ciency with impaired reproductive development [10–12]. *Corresponding author: Víctor Sánchez-Margalet, Department of
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14 Lee mas

Sam68 Mediates the Activation of Insulin and Leptin Signalling in Breast Cancer Cells.

Sam68 Mediates the Activation of Insulin and Leptin Signalling in Breast Cancer Cells.

Regarding the mechanism whereby Sam68 may mediate the activation of these pathways, it has previously been reported that Sam68 is associated with the SH3 domains of Grb2 in a constitutive way and may interact with the SH2 domains of GAP after insulin stimulation in HTC-IR cells [51] suggesting a role of Sam68 in the MAPK pathway. Moreover, the association of Tyr-phosphorylated Sam68 with the regulatory subunit of PI3K have been previously reported in hepatocytes and adipocytes in response to insulin [26] and in peripheral blood mononuclear cells in response to leptin [27]. This interaction may enhance the activation of PI3K pathway, which may support a role of Sam68 also in the activation of this pathway by these hormones. More importantly, IRS-1 is a key protein linking insulin and leptin stimulated PI3K and MAPK signaling pathways [64]. Sam68 has been previously demonstrated to interact with IRS-1 [65] according to the previously suggested role as adaptor protein in signal trans- duction in both leptin and insulin systems [8]. Since Sam68 seems to regulate IRS-1 expression, as we observed in the Sam68 down-regulation experiments, the role of Sam68 stimulating PI3K and MAPK signaling pathways may be mediated by IRS-1. As a consequence, the inhibi- tion of cell growth, either basal or insulin/leptin stimulated, may also be mediated by the inhi- bition of IRS-1 expression, since the down-regulation of IRS-1 is known to decrease cell growth rate [66]. Since Sam68 downregulation led to a decrease in both mRNA and protein content of IRS-1, the effect of Sam68 on IRS-1 expression should be at the transcription level. However, the mechanism whereby Sam68 may modulate IRS-1 expression is intriguing, and remains to be investigated.
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15 Lee mas

Immune Activation in HIV-treated Subjects and the Role of Age and Discordant Phenotype. A Cross-sectional Study.

Immune Activation in HIV-treated Subjects and the Role of Age and Discordant Phenotype. A Cross-sectional Study.

 1. Gazzola L, Tincati C, Bellistri GM, Monforte A, Marchet- ti G. The absence of CD4+ T cell count recovery despite receipt of virologically suppressive highly active antiret- roviral therapy: clinical risk, immunological gaps, and therapeutic options. Clin Infect Dis. 2009; 48(3):328-37.  2. Negredo E, Massanella M, Puig J, Pérez-Alvarez N, Gal- lego-Escuredo JM, Villarroya J ,et al. Nadir CD4 T cell count as predictor and high CD4 T cell intrinsic apopto- sis as final mechanism of poor CD4 T cell recovery in virologically suppressed HIV-infected patients: clinical implications. Clin Infect Dis. 2010; 50(9):1300-08.  3. Erikstrup C, Kronborg G, Lohse N, Ostrowski SR, Ger-
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7 Lee mas

Short Communication: Low expression of activation and inhibitory molecules on NK cells and CD4+ T cells is associated with viral control

Short Communication: Low expression of activation and inhibitory molecules on NK cells and CD4+ T cells is associated with viral control

The initial immune response during sexual exposure to HIV-1 is critical, because it defines whether the virus is eliminated at the mucosal site or if the infection is established. Several investigators have demonstrated the presence of genetic and immunological mechanisms that can reduce the risk of acquiring HIV-1 infection or limit its progression, including the presence of genetic polymorphisms in the viral co-receptors, innate and adaptive immune cells with particular phenotypic and functional features, and molecules such as antibodies and soluble factors that play an important role in defense against HIV-1 infection 8,18–23 . Moreover, some reports indicate that HESN individuals had a
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19 Lee mas

The role of leptin in obese children

The role of leptin in obese children

The obesity gene (ob) in mice encodes a protein produced by adipose tissue, leptin, which regulates body weight (3). Under experimental conditions, leptin affects the central nervous system and tends to reduce appetite and increase energy expenditure. Numerous studies have shown an increased expression of the ob gene (mRNA-leptin) in adipocytes or a marked increase in serum leptin concentration of obese subjects relative to lean subjects; a positive correlation with the body mass index has been reported (4,5). Leptin also exerts various effects on metabolism, glucose homeostasis and sexual development and activity. It has been reported that leptin serum levels do not merely reflect adipose tissue size but that they play in controlling of body weight homeostasis and fatness development. Some of these studies will be analyzed in this review, because the role for leptin to predict weight gain is still controversial.
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5 Lee mas

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