The laboratory data of the disease control were different from the other controls as he had undergone treatment with IVIG and aspirin. All blood samples were confirmed as blood group A, RhD positive. The laboratory findings HIF cancer during the disease course of case A are shown in Table 2. At day 30, ANC values were significantly decreased and platelet counts had contrastingly increased. The presence of autoantibodies to neutrophils was tested by D-GIFT and I-GIFT. D-GIFT was negative

in all subjects. Fig. 3B shows a representative I-GIFT result using the leukocytes of case C and the serum of case A. The M2 gate shows the levels of the neutrophil-associated antibody attaining an arbitrary level of fluorescence. No antibodies were present on day 5, before IVIG treatment. There was a direct correlation between increase in neutrophil-associated antibody levels and neutrophil counts of case A: as the amount of antibody increased, neutrophil counts of case A were further decreased, followed by an agranulocytic stage (serum on day 13 and day 30); then, as the amount of antibody gradually decreased, neutrophil

counts of case A increased, resulting in recovery from neutropenia (serum on day 64). Similar results were observed using different neutrophils (present case, control patient and other normal volunteers) with serum from the present case (case A). The percentage of cells within the M2 gate is LY2606368 chemical structure shown in Fig. 3C, which represents the changes in the relative antibody level and the ANC of the case A. The neutrophil counts of case A inversely correlated with the level of autoantibody Cyclin-dependent kinase 3 during the patient’s clinical course. No positive results using I-GIFT were observed among the serum from the disease or normal healthy controls. Examination of the same lots of immunoglobulin used for IVIG treatment also revealed an absence of antibodies to neutrophils. Neutropenia associated with KS patients is reported to be complicated with various autoimmune disorders [6]. In this study, an autoantibody to a novel antigen on immature myeloid cells or neutrophils

was produced in a patient with KS and revealed as the possible cause of severe neutropenia. In primary autoimmune neutropenia, the autoantibody specificity has been defined and the usually recognized human neutrophil antigens (HNAs) are located on glycosylated isoforms of FcγRIIIb (CD16b) [14, 15]. Autoantibody specificity associated with secondary autoimmune neutropenia is often unknown [16] but was recently shown to be associated with pan FcRγIIIb antibodies [17]. In this case, the recognized major HNAs were negative. We tried to evaluate the specificity of the immunoglobulin binding using an immunoblot technique with cell lysates to identity the target antigens. However, we could not identify the specific protein.

11–20 As the ablation of CD25-expressing cells almost uniformly augmented resistance with reduced recoverable in vivo pathogen

burden, Treg cells were appropriately described as ‘a dangerous necessity’ based on their detrimental roles in host defence and essential roles in sustaining immune tolerance.21 However, with the subsequent identification of Foxp3 as the lineage-defining marker for Treg cells, and the up-regulation of CD25 expression on activated T cells that occurs after infection, the conclusions of initial studies NVP-BGJ398 using CD25 expression as a surrogate marker for Treg cells deserve critical Selleck RG7420 re-evaluation using experimental strategies that identify and manipulate these cells based on Foxp3 expression. This review will summarize the recent literature describing infection outcomes and the immune response to infection using approaches that manipulate Treg cells based on Foxp3 expression, and frame these conclusions in the context of previous studies evaluating the importance of CD25+ CD4+ Treg cells and the epidemiology of human infection. Although an over-simplification, this analysis will be subdivided for pathogens that primarily cause acute versus persistent infection.

For each type of infection, the impacts resulting from the manipulation of Foxp3+ cells in infection outcomes, relevance of Foxp3+ Treg-cell antigen specificity and individual Foxp3+ cell intrinsic molecules in mediating immune suppression are discussed (Table 1). Lastly, how shifts in Treg-cell suppression Rolziracetam impact infection outcomes and our more basic understanding for how T cells are activated in vivo are also summarized. Pathogens that cause acute infection stimulate the activation of protective immune components almost immediately

after infection. When the pathogen dose or initial rate of pathogen replication are below a preset threshold (lethal dose), innate immune components keep the infection at bay until pathogen-specific adaptive immune effectors that more efficiently mediate pathogen eradication are expanded and mobilized. On the other hand, with higher inocula, these normally protective responses are overwhelmed and the host succumbs to infection. It is in this latter context that initial studies using Foxp3DTR transgenic mice that co-express the high-affinity human diphtheria toxin (DT) receptor with Foxp3, allowing Foxp3+ Treg cells to be selectively ablated with low-dose DT, first uncovered somewhat paradoxical protective roles for these cells in host defence.

Indeed, with Cry1Ac the response recorded in NALT is higher than those reported after immunization with CT B-subunit [18], with the surface protein of Streptococcus AgI/II [19], with

the antigen rBCG-V3J1 [20]; or using inactivated influenza vaccine coadministered with CTB [21], or with a vaccine containing fimbrial protein of Porphyromonas gingivalis NVP-LDE225 datasheet and CT [22]. Likewise, in NP the specific IgA antibody-producing cell responses elicited by Cry1Ac were superior to the responses generated using other antigens, such as OVA with CT [23], the antigen rBCG-V3J1 [20] and a vaccine with fimbrial protein of P. gingivalis and CT [22]. However, there is also evidence that other antigens induce a greater antibody-producing cell response than

the one induced with Cry1Ac in NP, such as NTHi a mucosal vaccine against Haemophilus FK866 solubility dmso influenzae coadministered with CT [24]. According to the majority of studies showing that intranasal immunization primarily triggers IgA antibody-producing cell responses [6, 25–28], we also found that with Cry1Ac or CT immunization, the IgA responses were the highest we recorded in both NP and NALT. However, it is important to mention that the IgG responses induced with these proteins at these nasal tissues also were significant. These observations coincide with other studies [18, 22, 29] that also have demonstrated that besides IgA, considerable IgG cell responses are locally produced in the nasal mucosa. In contrast, following intranasal immunization with rBCG-V3J1 vaccine [20], much higher V3-specific IgG than IgA-producing cell responses were found in several mucosa-associated tissues, including NALT, NP, PP and i-LP. Although the role of IgA in mucosal protection is well established, mucosal-associated IgG has also been shown to contribute to host defence [30–33]. So probably the responses of this isotype induced in click here NALT and NP might participate in mucosal protection as well. Furthermore, to our knowledge we have described here, for the first time, the effect of intranasal immunization on the expression

of the activation markers CD25 and CD69 in NALT and NP lymphocytes. Our data indicate that Cry1Ac is effective in inducing activation of B and T cells in both NALT and NP. However, the activation markers were differentially induced. Whereas the expression of CD25 was increased in B cells, as well as in CD4+ and CD8+ T cells from NALT and NP, CD69 was increased in B cells from both compartments but only in CD4+ T cells from NP. The expression of CD25 and CD69 is characteristic of highly activated T cells. Certainly, in lung airways, it has been shown that substantial numbers of virus-specific CD4 and CD8 T cells expressing these activation markers can be recovered more than 1 year after resolution of either an influenza or Sendai virus infection [34–36].

Polymorphisms in the IL-1 receptor antagonist gene (IL1RN) and TNF have been associated with susceptibility to IPF

[6,7]. Several studies suggest that IL-1β and IL-1Ra play a critical role in bleomycin-induced fibrosis in mice. CYC202 order Fibrosis is induced by IL-1β and neutralization of IL-1β by antibodies or specific blockage of the receptor IL-1R1 reduces the development of fibrosis [8]. In normal homeostasis, IL-1Ra production by alveolar macrophages is higher than the production of IL-1β. However, decrease in the ratio of IL-1Ra to IL-1β favours the augmentation of the pro-fibrotic function of IL-1β[9]. The aim of this study was to investigate both the predisposition and disease-modifying effects Dorsomorphin mw of genetic variations in the IL1B and IL1RN genes and corresponding proinflammatory cytokine levels in serum and bronchoalveolar lavage fluid (BALF) in a cohort of IPF patients. Patients with IPF presenting at the Department of Pulmonology of the St Antonius Hospital in Nieuwegein between 1998 and 2007 were included in this study. From that time serum, BALF and DNA were collected from all interstitial lung disease (ILD) patients presented at our department after informed consent was given. These patients were enrolled in our database for scientific research. Retrospectively, the diagnosis of

IPF was reviewed and validated using current American Thoracic Society/European Respiratory Society (ATS/ERS) guidelines. Diagnoses made before 2002 were reviewed by an experienced clinician (J.v.d.B., J.G.), and G protein-coupled receptor kinase patients were included only when current ATS/ERS criteria were met. Other causes of usual interstitial pneumonia (UIP) (drugs, collagen vascular diseases) were ruled out. Seventy-seven IPF patients [mean age 60·8 years, standard deviation (s.d.) 13·6, 58 males, 19 females] were included in the present study and donated DNA. In 54 of 77 cases serum and BALF samples were also available at the time of

diagnosis. At the time of serum sampling eight patients received low-dose oral corticosteroids. In 58 cases the diagnosis of UIP was confirmed on lung biopsy (75%). BALF was collected as described previously [10]. Samples were stored at −80°C until analysis. Median lung function parameters at the time of diagnosis were as follows: forced vital capacity (FVC) 75·7 % predicted [interquartile range (IQR) 61·7–87·3], DLCO 42·5 % predicted (IQR 33·1–55·6). The control group consisted of 349 healthy Caucasian volunteers (mean age 39·2 years, s.d. 12·4, 139 males, 210 females). In 36 cases in the control group, BAL was performed and in those controls cytokine levels in serum and BALF were measured. The study protocol was approved by the Ethical Committee of the St Antonius Hospital and all subjects gave written informed consent.

Additionally, CTLA-4-Ig has been shown to induce production of indoleamine 2,3-dioxygenase

(IDO) from APCs, which would inhibit T cell activation by tryptophan depletion [27, 28]. Another potential immunosuppressive mechanism has been suggested by which CTLA-4-Ig can induce and increase the population of regulatory T cells both in this website vitro [29] as well as in collagen-induced arthritis in mice [30]. In this study, we have shown further that activation and proliferation of T cells in the sensitized draining lymph node are inhibited after treatment with CTLA-4-Ig and that infiltration of activated effector CD8+ T cells in the inflamed tissue is reduced after challenge. The effect in the draining lymph node is in accordance with a study performed by Platt et al. [26], who demonstrated that in an ovalbumin (OVA)-specific T cell activation model, CTLA-4-Ig treatment leads to a reduced proliferation of T cells and reduced down-regulation of CD62L on OVA-specific T cells 3 days post-immunization together with a reduced expression of CD69 1 day post-immunization [26]. Less efficient down-regulation of CD62L on T cells in CTLA-4-Ig-treated mice is consistent with a reduced infiltration of effector cells into

the inflamed ear tissue, as down-regulation of Selleck Tamoxifen CD62L is needed for lymphocytes to Axenfeld syndrome exit the draining lymph node and to enter the site of inflammation [31]. Further, our data suggest that CTLA-4-Ig binds primarily to DCs but also mediates a strong inhibition of CD86 expression on B cells. Cytokines IL-4 and IL-1β, together with chemokines MIP-2 and IP-10, were suppressed after CTLA-4-Ig treatment. In the skin, a major source of both MIP-2 and IP-10 is keratinocytes

[32, 33] and it is currently not known how CTLA-4-Ig may suppress production of these two chemokines. It has been suggested that IP-10 production from keratinocytes attracts CD8+ T cells, which subsequently secrete IFN-γ, further stimulating keratinocytes to produce more IP-10 and thereby completing a positive feedback loop [34]. Because CTLA-4-Ig inhibits infiltration of CD8+ T cells into the challenged ear it is possible that the reduced infiltration of CD8+ T cells could lead to decreased release of IP-10, as found in our analysis. The data in the adoptive transfer studies show that both IP-10 and MIP-2 are suppressed when CTLA-4-Ig is present only in the sensitization phase – this is expected, as the presence of CTLA-4-Ig in the sensitization phase only also results in a reduced ear swelling and reduced influx of CD8+ T cells (Figs 4 and S2). However, it was surprising that MIP-2 but not IP-10 was suppressed when CTLA-4-Ig was present in the challenge phase alone, which does not reduce ear swelling (Fig. S2).

In sensitized group, the mast cells were much bigger, with more shrink on the cell membrane, bubbles in the cytoplasm and degranulation vehicles around the cells check details (Fig. 2A). Furthermore, ultrastructure analysis of mast cells by transmission electron microscope showed that the cell membrane was obscure, and degranulation vehicles was less evenly distributed in the cytoplasm of mast cells (Fig. 2A). The number of mast cells was significantly increased in OVA-treated RPLS (Fig. 2B). The

ratio of mast cell degranulation as indicated by vehicles (at least five) around the cells was also dramatically increased by ~3 fold (Fig. 2B). Mast cell degranulation was further confirmed by increased histamine levels in serum and RPLS (Fig. 2C). It has been suggested that an increase in intracellular Ca2+ through SOC channel is essential for mast cell degranulation

[13]. We therefore examined whether food allergen–induced mast cell activation is related to stimulation of Ca2+ mobilization. As shown in Fig. 3, the TG-evoked Ca2+ influx was dramatically enhanced in OVA-sensitized rat peritoneal mast cells, suggesting mast cell activation in the food-allergic model is related to upregulation of Ca2+ entry through SOCs. STIM1 and Orail are the two subunits of SOCs [23, 24]. Overexpression of STIM1 and Orail caused a significant increase in store-operated Ca2+ entry in RBL cells [16]. We thus examined the see more expression levels of both subunits. The results show that the mRNA (Fig. 3A,B) and protein levels Ketotifen (Fig. 3C,D) of both subunits were significantly increased in allergic animals as compared with controls (all P < 0.01). Furthermore, immunofluorescence study revealed that

the STIM1 subunits were translocated to the cell membrane, which is required for the activation of SOCs in OVA group, while it was evenly distributed in cytoplasm in control group (Fig. 4). Collectively, these data indicate that OVA-induced food allergy increased SOCs activity by enhancing transcription and expression of SOCs subunits, as well as increasing SOCs activity. Reactive oxygen species production in RPMCs isolated from control or allergic animals was examined by ELISA. The results demonstrated that ROS production in allergic mast cells was increased by 1.5-folds as compared with controls (Fig. 5A). Administration with ROS scavenger Ebselen (100 μm, 30 min) to OVA-challenged RPMCs reduced ROS production by ~30% (Fig. 5A). In parallel, clearance of intracellular ROS by Ebselen decreased histamine release by ~30% (Fig. 5B). Similarly, OVA challenge–induced Ca2+ increase through SOCs in activated mast cell was decreased by 30% by Ebselen treatment (Fig. 5C,D). The results indicate that mast cell activation is partially attributed to increased ROS production. Quantification of the protein levels of Orai1 and STIM1 demonstrated that Ebselen reduced both protein expressions by ~40% and ~30%, respectively (Fig.

, 2007). OD values were evaluated at 490 nm by a plate reader (Synergy HT, Bio-TEK). Data were expressed as the stimulation index, calculated

as the mean reading of triplicate wells stimulated with antigen divided by the mean reading of triplicate wells stimulated with medium. Intracellular cytokine staining was performed as previously described (Wang et al., 2008). Briefly, single T-cell suspension from each group at 1 × 106 cells/100 μL was stimulated in a 96-well plate with HBsAg (5 μg mL−1) for 6 h, and treated with monensin (2 μg mL−1, eBioscience, San Diego, CA) for the last 4 h. Cells were blocked with Fc-Block (BD Phamingen, San Diego) for 30 min. Cells

were fixed with 4% paraformaldehyde for 15 min before permeabilization with 0.1% saponin for 10 min. The cells PI3K inhibitor were stained with isotype controls, or double stained with anti-CD8-PE plus anti-IFN-γ-FITC, anti-CD4-PE and anti-IFN-γ-FITC, anti-CD4-PE plus anti-IL-2-FITC, or anti-CD4-FITC plus anti-IL-4-PE for 30 min. The cells were detected by a FACS Calibur and analysed using cellquest pro Software (BD Bioscience). The frequency of CD4+CD25+Foxp3+ Treg cells was tested with the mouse regulatory T-cell staining kit according the manufacturer’s instructions (eBioscience). An in vivo cytotoxicity assay was performed as described previously (Zou et al., 2010). Single suspension cells from Selleck Romidepsin naive BALB/c mice were split equally into two portions. One portion as the target cell was labeled with 5 μM CFSE carboxyfluorescein Protirelin diacetate, succinimidyl ester (Fan-bo biochemiscals, Beijing,

China; CFSEhigh) after being pulsed with the CTL peptide S208-215 (50 μg mL−1) for 4 h. The other portion as a nontarget control and was labeled only with 0.5 μM CFSE (CFSElow). The two portions were mixed in a 1:1 ratio and injected into immunized mice at 2 × 107 total cells per mouse via the tail vein on day 7 after the second immunization. Splenocytes were isolated 4 h later and the CFSE-labeled cells were tested by a FACS Calibur analyser based on their different CFSE fluorescence intensities. Specific lysis was calculated according to: % specific lysis = [1 – (% specific peptide-loaded target cells/% control peptide-loaded target cells)] × 100%. Total RNA was extracted from splenocytes of immunized mice with Trizol reagent (Invitrogen, Carlsbad, CA) according to the manufacturer’s instructions. cDNA was synthesized using Ace reverse transcriptase (Toyobo Co. Ltd, Pudong, Shanghai) with Oligo (dT) 18 primers (the primers for PCR are listed in Table 1). PCR products were resolved on 1.5% agarose gels and visualized by ethidium bromide staining under UV light.

The authors thank Dr. Derek Abbott and Jill Marinis for help with the Western blots and H&E staining of abscess sections. The authors also thank Nile Chang and Dr. Alex Huang for assistance with cryosections and for use of Imaris image analysis software and Dr. Lakshmi

Ramachandra for providing LADMAC-derived macrophages. This work was funded by grants to B. A. Cobb (NIH, AI062707 and NIH, OD004225 and CGD Research Trust, Grant ♯ J4G/06/01). Conflict of interest: The work described herein is the subject of a provisional patent BIBW2992 cost application (♯61332896) filed with the United States Patent and Trademark Office governing the use of 1400W in abscess prevention in CGD and other patients at risk for abscess formation. “
“The isolation of lymphocytes and other hematopoietic-derived cells from small intestinal tissues has become increasingly relevant to immunology over the last decade. find more It is also becoming increasingly clear that the impact of local immunity at the mucosal barrier of the intestine has a profound impact on immune responses at distant sites, bringing a new cadre of immunologists to the mucosal frontier. Furthermore, the ability to experimentally manipulate

smaller and smaller populations of immune cells has become technologically feasible and in some cases routine. The expanding importance of mucosal immunology coupled with increased technical capabilities requires a standard for experimentally obtaining uniform selleck products and consistent cells from the intestinal mucosa. Therefore, it is important to isolate immune cells that are highly viable and

minimally manipulated to maximize cellular yields while maintaining acceptable time constraints. Curr. Protoc. Immunol. 99:3.19.1-3.19.11. © 2012 by John Wiley & Sons, Inc. “
“Activating and inhibitory killer immunoglobulin-like receptors (KIR) and their ligands HLA-Bw4 (loci A and B) were studied by way of establishing whether they can contribute to protection against HIV-1 infection in highly exposed and persistently seronegative (HESN) patients. Twenty-three HIV-1 serodiscordant heterosexual couples, 100 HIV-1+ patients and 200 healthy individuals were included in this retrospective case–control study. HLA typing was performed by means of PCR followed by sequence-specific oligonucleotide probe reverse hybridization. KIR3DL1 and KIR3DS1 were studied by PCR sequence-specific primers. The frequency of KIR3DS1(3DS1/3DL1)-Bw4 combination was significantly higher in HESN patients versus the discordant couples (P = 0·0003) and HIV-1+ patients (P = 0·0001). Conversely, the KIR3DL1/KIR3DL1 homozygosity was significantly decreased in HESN patients versus the discordant couples (P = 0·00003), and HIV-1+ patients (P = 0·00066). The frequency of HLA-A*32 and HLA-B*44 was higher in HESN versus their discordant couples (P = 0·009; P = 0·049), and HIV-1+ patients (P = 0·00002; P = 0·0001).

47–49 The interaction between T cells and macrophages

is known to be critical for prevention of bacterial growth.50–53 However, it is not clear how various M. tuberculosis proteins can trigger the Th1 response. Several factors, such as the affinity between the T-cell receptor (TCR) and peptide–MHC ligand, peptide ligand density and costimulatory signalling during T-cell activation, can play important roles BTK inhibitor in the regulation of the Th1/Th2 T-cell response.11,12,54–57 Cytokines induced during innate activation of macrophages have also been shown to be extremely important in controlling the Th1/Th2 balance. For example, induction of IL-12 or TNF-α can trigger a Th1 response;58,59 however, if more IL-10 is produced, the response is likely to be biased towards the Th2 type response.60,61 It has been shown that various M. tuberculosis

secretory proteins bind to a specific receptor on macrophages and influence the downstream signalling cascades and the induction of pro-inflammatory cytokines.62 Although up-regulation of iNOS expression and NO production during infection with M. tuberculosis is well known, very few studies have actually identified the M. tuberculosis proteins directly involved in the up-regulation of the iNOS gene. Our study indicates that rRv2626c affects the macrophage-signalling cascades Temsirolimus and up-regulates iNOS induction and NO production mainly by increasing NF-κB activity. Interestingly, flow cytometry data indicate that Rv2626c binds to the macrophage surface with high affinity and specificity. It is possible that the specific binding of Rv2626c on the macrophage surface causes modulation of the downstream signalling pathways triggering NF-κB signalling, which results in increased induction of iNOS23 as well as the cytokines TNF-α63 and IL-12.64 Although the exact beneficial role of iNOS/NO in anti-mycobacterial Erastin killing has not been uniformly elucidated,65 studies have confirmed that iNOS/NO is crucial in limiting bacterial growth.66,67 Similarly, the role of TNF-α in TB is paradoxical because, although there is evidence of its protective role,68 it can play a part in the tissue damage that

characterizes human disease.68 A recent study also indicates that M. tuberculosis activates TNF-α production to induce apoptosis of macrophages.62 Our study clearly demonstrates that the secretory M. tuberculosis Rv2626c protein induces pro-inflammatory responses by modulating the expression of iNOS and increasing the secretion of IL-12 and TNF-α, which may play an important role in the initiation of the adaptive immune response in the host. Mycobacterium tuberculosis proteins that induce the Th1 response have been used as targets for subunit vaccines. For example, use of the mycobacterial 30-kDa major secretory protein (antigen 85B, Ag85B) was found to protect animals from M. tuberculosis infection by inducing a Th1-dominant response.

We discuss the clinical and experimental evidence that supports the notion that the microcirculation, specifically cell-to-cell communication, likely contributes to the development of VaD. Through exploration of the concept of the NVU, we elucidate

the extensive cerebrovascular communication that exists and highlight models that may help test the contribution(s) of cell-to-cell communication at the microvascular level to the development and progression of VaD. Lastly, we explore the possibility that some dementia, generally considered to be find more purely neurodegenerative, may actually have a vascular component at the neurovascular level. Conclusion:  This latter recognition potentially broadens the critical involvement of microvascular events that contribute to the numerous dementias affecting an increasingly larger sector of the adult population. “
“Cell–cell adhesion complexes are increasingly recognized as an important cell-signaling site, similar to integrin-extracellular matrix FA. Furthermore, cell–cell adhesions are involved in the regulation

of multi-cellular/tissue organization and organ, tissue, and cellular level functional behavior. Although N-cadherin is the major cell–cell adhesion molecule in VSM, only limited studies have been undertaken to understand its function in VSM. Nutlin-3a cell line In contrast, N-cadherin signaling and functions have been extensively studied in neurons, fibroblasts, and myocytes, as well as in the context

of epithelial-mesenchymal-transitions. Increasing evidence has indicated Sulfite dehydrogenase that N-cadherin-mediated cell–cell adhesions are important for tissue integrity and cell proliferation. Relevant to VSM, N-cadherin’s role in actin cytoskeleton organization and contraction, as well as its role in regulation of Rho family GTPases are of particular interest. This article briefly reviews the fundamentals of N-cadherin biology that help shape our current understanding of its function and signaling mechanisms. In particular, attention is given to applications of this knowledge to VSM. The review points to the need for more research effort that is directed at understanding the role of N-cadherins in the regulation of vascular function. “
“Please cite this paper as: Wang, Hein, Zhang, Zawieja, Liao and Kuo (2011). Oxidized Low-Density Lipoprotein Inhibits Nitric Oxide-Mediated Coronary Arteriolar Dilation by Up-regulating Endothelial Arginase I. Microcirculation18(1), 36–45. Oxidized low-density lipoprotein (OxLDL) causes impairment of endothelium-dependent, nitric oxide (NO)-mediated vasodilation involving l-arginine deficiency. However, the underlying mechanism remains elusive. Since arginase and endothelial NO synthase (eNOS) share the substrate l-arginine, we hypothesized that OxLDL may reduce l-arginine availability to eNOS for NO production, and thus vasodilation, by up-regulating arginase.