The induction of IFN-γ synthesis in the female genital tract is necessary for the induction of an immune response, and subsequent sensitization, of the female to spermatozoa (Witkin, 1988). It is intriguing to speculate whether perhaps an additional function of lactic acid downmodulation of Th1 cell formation in the vagina may be to help preserve fertility

by limiting an IFN-γ response to commensal bacteria and to microorganisms transmitted in the male ejaculate. S.S.W. designed the study, analyzed the data and prepared the original manuscript. S.A. and A.M.B. performed the experiments GDC-0449 nmr and collected data. I.M.L., W.J.L. and A.M.B. participated in data analysis. W.J.L. and I.M.L. participated in the final manuscript

check details preparation. All of the authors read and approved the final manuscript. “
“The effect of IFN-γ on the expression of osteopontin (OPN), in the presence or absence of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3), in decidual stromal cells (DSC). Decidual stromal cells were isolated from women undergoing elective termination of pregnancy (gestational age, 6–9 weeks). After characterization, they were treated with IFN-γ in the presence or absence of 1,25(OH)2D3. The uterus of pregnancy IFN-γ knockout mice were collected on gestation day (gd) 7.5, and the expression of OPN were examined. IFN-γ drastically decreased the expression of OPN in DSC, which was reverted by the addition of 1,25(OH)2D3 to the IFN-γ-treated decidual cells. Moreover, the OPN expression in uterus of IFN-γ knockout mice was higher than that of wild-type Sclareol counterparts. We demonstrated OPN was expressed in DSC in human first-trimester decidua and in the uterus in mice at 7.5 gd. The OPN expression was closely correlated with regulation of IFN-γ and 1,25(OH)2D3 in human early pregnancy. OPN expression in DSC was significantly decreased with the treatment of IFN-γ. 1,25(OH)2D3 played an opposite role in IFN-γ-mediated inhibition of OPN expression in human DSC. “
“Chlamydia trachomatis serovars D-K are obligate intracellular

bacteria that have tropism for the columnar epithelial cells of the genital tract. Chlamydia trachomatis infection has been reported to induce modifications in immune cell ligand expression on epithelial host cells. In this study, we used an in vitro infection model that resulted in a partial infection of C. trachomatis-exposed primary-like immortalized endocervical epithelial cells (A2EN). Using this model, we demonstrated that expression of the natural killer (NK) cell activating ligand, MHC class I-related protein A (MICA), was upregulated on C. trachomatis-infected, but not on noninfected bystander cells. MICA upregulation was concomitant with MHC class I downregulation and impacted the susceptibility of C.

Both methods present advantages and disadvantages. In solid pieces of tissue, neurones are mixed together check details with glial populations, which could help the maturation of the tissue in the host brain [145]. Importantly, with the latter approach, cells do not undergo mechanical stress, trauma or necrosis due to axotomy, although cell death may still occur upon dissection

of the tissue [146]. On the other hand, cell suspensions, which require the mechanical dissociation of the tissue with potential accompanying cell damage, are surgically easier to implant in the brain. Dissociated cells are also more likely to be integrated in the host brain and to form afferent and efferent connections with the latter [147]. However, the trituration of the tissue leads to the destruction of the donor vasculature leaving the graft to rely strictly on the vascular supply of the host [90,148,149]. Solid pieces R788 ic50 of tissue maintain their own angioarchitecture and will more readily anastomose with surrounding vessels [114,148,150,151]. Finally, cell suspensions trigger a weaker inflammatory response, in part because they are injected through a smaller cannula than solid grafts [139]. In clinical trials, the cell suspensions utilized were not completely dissociated and small clusters of cells were maintained, introducing a source of variability with regard to the effective number of cells implanted

between transplants. However, the method of cell suspension seems to yield a better outcome [139]. The regime of immunosuppression is another parameter that may be predictive of graft outcome and one that is intermingled with the cellular and molecular immune/inflammatory responses against grafted tissue (Table 1).

The early work on transplantation in animal models of disease demonstrated that the long-term survival of dopaminergic xenografts (mouse to rat and human to rat) was improved when the immunosuppressive drug cyclosporine A was administered to the recipient animal, even for a short period of time [152,153]. However, halting cyclosporine treatment reduced functional effects of grafted tissue at later time points (6 months), although the improvement of the behavioural phenotype of the immunosuppressed animals was still greater than in non-immunosuppressed 3-oxoacyl-(acyl-carrier-protein) reductase animals [154]. Clinically, the withdrawal of immunosuppression coincided with the decline of beneficial effects in PD patients [155]. It was suggested that this could reflect graft rejection, although grafts survival was confirmed both by PET scans of Fluoro-dopa uptake and later by post-mortem histological analysis [155], similarly to previous reports [156]. In other PD cases, the withdrawal of the immunotherapy treatment did not lead to graft rejection [157,158]. Two independent reports have further described grafts survival in the absence of any immunosuppressive treatment [109,159].

There will be a group of seven Executive Editors representing a wide range Protein Tyrosine Kinase inhibitor of specialist interests and they will handle the review process for papers. The Editorial Board will be expanded enabling the review of a larger proportion of papers within the Board. Where good quality papers are judged to be unsuitable for publication in Neuropathology and Applied Neurobiology authors will be offered the option that these are forwarded, together with the reviews, to the Wiley open access journal Brain and Behavior. Our readers remain in the focus and for them we must provide

novel, insightful and relevant papers with a broad approach to neuropathology and neuroscience. Accessibility of published material is important and Neuropathology and Applied Neurobiology participates in the Wiley-Blackwell Open Access program, OnlineOpen. Wiley-Blackwell also makes Neuropathology and Applied Neurobiology available to institutions in a number of developing countries at reduced, or no cost, supporting scientists from all backgrounds. Our comprehensive review papers and, in particular, the annual review EMD 1214063 edition, have proved extremely popular with readers and these will continue. A new

venture for the Journal is the appointment of a Social Media Editor and I welcome Dr Abi Li to this position. It is vital that we engage in new approaches to promote access and awareness of the Journal and its content 5 FU to a global readership, we will be at the forefront of such developments. “
“M. Hasselblatt, B. Riesmeier,

B. Lechtape, A. Brentrup, W. Stummer, F. K. Albert, A. Sepehrnia, H. Ebel, J. Gerß and W. Paulus (2011) Neuropathology and Applied Neurobiology37, 803–806 BRAF-KIAA1549 fusion transcripts are less frequent in pilocytic astrocytomas diagnosed in adults Aim: Duplication of 7q34 resulting in generation of BRAF-KIAA1549 fusion transcripts is a characteristic event in pilocytic astrocytoma that may also aid distinction from diffuse astrocytic tumours. As data on BRAF-KIAA1549 fusion transcript status remain mainly limited to children, we aimed to examine the diagnostic value of BRAF-KIAA1549 fusion transcripts across all age groups. Methods:BRAF-KIAA1549 fusion transcript status was examined using reverse transcription polymerase chain reaction on formalin-fixed paraffin-embedded samples of 105 primary pilocytic astrocytomas [median patient age: 17 years (1–74 years)]. Results: Informative results (distinct wildtype BRAF bands detectable) were obtained in 105/124 cases (85%). Fusion transcripts were detected in 53 of cases (51%). They were more often encountered in tumours of infratentorial location [42/67 (63%) vs. 11/38 (29%)] and comprised KIAA1549-Ex16_BRAF-Ex9 (32 cases), KIAA1549-Ex15_BRAF-Ex9 (14 cases) and KIAA1549-Ex16_BRAF-Ex11 (seven cases).

Recently, OXA-48-producing E. coli identified in France from patients transferred from Egypt were described [16]. Our findings thus confirm the hypotheses about a likely endemic LBH589 molecular weight circulation of OXA-48 in Egypt and other north African countries [16]. Of special interest, the carbapenem-resistant isolate of phylogroup B1 containing blaCMY-2, blaOXA-48 and blaVIM-29 was attributed with ST101. This supports the concerning evidence of a previous study by Mushtaq et al. who reported that 9/18 isolates of NDM-producing

E. coli from England, Pakistan and India were B1-ST101 [17]. Finally, ciprofloxacin resistance was associated with the presence of qnrS in only two phylogroup A isolates, whereas in all the remaining strains aac(6′)-Ib-cr was detected (Table 1). Twenty of 27 ciprofloxacin resistant E. coli isolates showed an association with blaCTX-M-15 and aac(6′)-Ib-cr genes. Thus, the genetic makeup which has driven the success of the ST131 pandemic clone appears to be diffuse among E. coli strains of different lineages and habitats. Acquisition of multidrug resistance gene traits by a widely disseminated human commensal organism on a global scale may seriously affect human health INCB024360 cell line and healthcare resources by causing difficult-to-treat infections in both community and healthcare settings, thus increasingly fueling the antibiotic crisis [1, 2]. The impact may be devastating in limited resource countries

and immunocompromised hosts, such as cancer patients. A previous report from Egypt described rates of resistance to third generation cephalosporins of approximately 60%in bloodstream isolates of E. coli from five hospitals in Cairo, Egypt in 1999–2000 [18]. Our findings confirm an alarming picture of multidrug resistance in E. coli and highlight acquisition of a variety of resistance genetic determinants in association with PMQR genes and the emergence of resistance to carbapenems. This work was financially supported by Institutional funds of the Department of Sciences for Health Promotion and Mother-Child Care “G. D’Alessandro. The authors declare no potential conflicts of interest with respect to the research, authorship,

and/or publication of this article. “
“The reports on fish parasite Anisakis simplex allergy have increased in countries with high fish consumption in the last decade. next In Norway, a high consumption country, the prevalence of immunoglobulin E (IgE) sensitisation to A. simplex was still unknown. Thus, our objective was to investigate the sensitisation prevalence in this country. At the Haukeland University Hospital, Bergen, Norway, two main groups of surplus serum samples were collected; one from newly recruited blood donors, and one from the Allergy laboratory after analysing IgE and IgE antibodies. The latter was divided into three series, one containing unsorted sera, and two sorted either by Phadiatop®≥ 0.35 kUA/L or total IgE ≥ 1000 kU/L. The sera were analysed for total IgE and IgE antibodies against A.

Equally interesting, however, is the observation that these changes do not take place in all cell types: in particular, CD14+ cells show a pattern that is consistent with an inhibition of the first phase of this process, suggesting

that in patients Nutlin3a with active TB, the extrinsic apoptotic pathway is strongly activated, but that monocytic cells may become less responsive to TNF-α or Fas-mediated lysis and thus less likely to be driven to apoptosis. If apoptosis is in fact playing a role in the containment of the bacteria by the removal of infected cells, these data may explain both why anti-TNF-α therapy has such a profound reactivating effect on latent TB infection and also why – if TNF-α is essential for protection – M. tuberculosis-infected individuals can still progress to TB in the face of greatly elevated TNF-α production. Participants (index cases, designated Index, n=27) in the study were recruited when sputum-positive

TB patients were identified at local TB clinics. We also recruited those close household contacts (healthy household contacts designated HHC, n=70) and CC (n=29) from the same area. Both HHC and CC by definition had no symptoms or suspicious X-ray findings. Blood was drawn at entry to the study, and half used for isolation and MACS separation of PBMC, followed by lysis and mRNA extraction. Plasma was also isolated from these GSK2126458 samples. The second half was lysed and mRNA extracted without separation. The mRNA was reverse transcribed into cDNA and this was used for all subsequent analyses. Since TNF-α is an important initiator Rapamycin of cell death via the extrinsic pathway and has been implicated in mycobacteria-induced cell death 38, we initially compared the expression of mRNA for TNF-α, TNFR1 (p55) and TNFR2 (p75). As seen in Fig. 1A–C, mRNA for all three

markers was elevated in cells from whole blood from TB patients. In household contacts of these sputum-positive index cases, mRNA for TNF-α (but not that of the receptors) was also significantly elevated, consistent with earlier published results showing elevated TNF-α expression in newly diagnosed TB patients 5. To analyze the response on a per-cell basis, we separated PBMC from the three cohorts into CD14+ (monocyte-containing) and CD14− (non-monocyte-containing) subsets using MACS. As shown in Fig. 1D and G, when analyzed on a per-cell basis, TNF-1 expression was not significantly different between the cohorts, for either the CD14− (T-cell-containing) or CD14+ (monocyte-containing) fractions. With regard to the TNF-1 receptors, however, the picture is quite different. In this case, the monocytic fraction of PBMC from TB patients expressed significantly lower levels of mRNA for TNFR1 and TNFR2 per cell than the monocytic fraction from CC, whereas no difference was seen in per-cell levels in the non-monocytic component (Fig. 1E, F, H and I).

[35]. Subsequently, the sections were rinsed again

in TBS and coverslipped with glycerol/gelatin (Sigma). Alternatively, sections were rinsed with TBS, briefly washed with distilled water, mounted onto glass slides, air-dried and coverslipped with Entellan in toluene (Merck, Darmstadt, Germany). Control experiments were performed by omitting the primary antibodies or switching the fluorophores related to the different markers. All calculations were performed using GraphPad Prism version 5.01 (GraphPad Software, San Diego, CA, USA). Differences between Saracatinib order groups were checked for significance using one-way analysis of variance (anova) with Bonferroni post hoc test, or unpaired t-tests. Data are shown as mean ± SEM. Significance levels were determined as follows: *P < 0.05, **P < 0.01. Prior to immunolesioning experiments with 12-month-old mice, the occurrence of AD-like alterations in this age group had been verified. Concomitant β-amyloidosis and allocated hyperphosphorylated tau were revealed by double fluorescence labelling of hippocampal sections with antibodies recognizing total Aβ and the established marker for phospho-tau, AT8 (Figure 1a). Additionally, the combined staining of APP and 4G8 (raised against Aβ17–24, but with reported cross-reactivity for APP [36]) resulted in strong red fluorescent APP immunosignals and numerous

green fluorescent 4G8-monolabelled deposits, but also a portion of yellowish appearing structures immunopositive for both markers (Figure 1b). The efficacy of immunolesioning in 16-month-old

this website mice that underwent icv immunotoxin injection 4 months before was routinely analysed by immunofluorescence labelling with affinity-purified goat-anti-ChAT as a marker for cholinergic neurones. Thereby, ChAT immunolabelling revealed the expected cholinergic chemoarchitecture in the forebrain of age-matched untreated control mice, e.g., the basal forebrain projection neurones and the more laterally located striatal interneurones (Figure 2a), which was not distinguishable from the staining Selleck Pembrolizumab of cholinergic cells in mice 4 months after sham-injection with anti-p75 (Figure 2b). In contrast, 16-month-old immunolesioned mice were nearly devoid of ChAT-immunopositive neurones, whereas the respective striatal staining remained (Figure 2c). Additionally, selected sections containing the MS/DB were applied to p75 immunolabelling; thereby, forebrain sections from naive animals (Figure 2d) and from mice that had underwent sham-injections (Figure 2e) appeared nearly identical, i.e. the CPN neurones displayed the expected staining, whereas the striatum was devoid of p75-immunoreactivity. On the other hand, after successful immunolesion nearly no p75-immunoreactivity of CPN remained (Figure 2f).

Finally,

XBP-1 regulates IgH transcription indirectly through induction of OBF1, a transcriptional co-activator for IgH [94]. These data seem to point to the hypothesis that activated B cells get prepared to handle high amount of immunoglobulins in a preemptive manner. The presence of misfolded Ig chains amplifies the UPR signalling, but it seems that the pathway is activated before nascent chains appear. We propose a model where Blimp1 expression derepresses XBP1 and the IRE1α/XBP-1 axis is activated in a differentiation-dependent manner. Expression of XBP-1s prepares the cells to handle high levels of Ig synthesis, while misfolded nascent chains amplify the pathway signalling at a later stage. Moreover, expression of ATF6 helps the cell sustain the demands for increased production of antibodies (Fig. 4). So far, this model raises more Neratinib research buy questions than answers. How the differentiation programme triggers the IRE1α/XBP-1 axis? Do cytokines and/or inflammatory millieu interfere with IRE1α/XBP-1 activation? Future data from several groups is awaited with excitement. Meanwhile, it is undeniable that the ability to properly fold and secrete proteins has revealed to Wnt inhibitor review be an important

restrictive aspect for the development of both innate and adaptive immune responses. As we learn more about it, it is conceivable to wonder whether we should begin to think about questions such as hypogammaglobulinemia and lymphocyte differentiation as protein folding dynamics issues. The authors thank Drs. Aguinaldo R. Pinto and Laila A. Nahum for critical reading of this manuscript and acknowledge the support Dapagliflozin of the agency FAPESP (09/06529-8 to S.E.A.R. and 09/51326-8 to M.M.D.C.). “
“The immune system is intricately regulated allowing potent effectors to expand and become rapidly mobilized after infection, while simultaneously silencing potentially detrimental responses that averts immune-mediated damage to host tissues. This relies in large part on the delicate interplay between immune suppressive regulatory CD4+ T (Treg) cells and immune effectors that without active suppression by Treg cells cause systemic and organ-specific autoimmunity. Although these beneficial

roles have been classically described as counterbalanced by impaired host defence against infection, newfound protective roles for Treg cells against specific viral pathogens (e.g. herpes simplex virus 2, lymphocytic choriomeningitis virus, West Nile virus) have been uncovered using transgenic mice that allow in vivo Treg-cell ablation based on Foxp3 expression. In turn, Foxp3+ Treg cells also provide protection against some parasitic (Plasmodium sp., Toxoplasma gondii) and fungal (Candida albicans) pathogens. By contrast, for bacterial and mycobacterial infections (e.g. Listeria monocytogenes, Salmonella enterica, Mycobacterium tuberculosis), experimental manipulation of Foxp3+ cells continues to indicate detrimental roles for Treg cells in host defence.

The novel use of a known therapy – fecal microbiota transplantation has shown promise in recurring and refractory cases, with minimal complications in this susceptible population, as we illustrate in this case of a renal transplant recipient. Case description: We report the case of a 62yr deceased donor renal transplant learn more recipient on standard immunosuppression, who had multiple hospital admissions either as a result of, or complicated by CDAD. She was treated with specific antibiotics (vancomicin, metronoidazole, rifaximin and fidaxomicin; multiple courses) but proved to be refractory to medical therapy. She had a total of 20 hospital admissions across the health district in the period

from October 2011 to February 2014, resulting in a total of 397 days spent in hospital, during which she always developed CDAD. Osimertinib in vivo She underwent a fecal microbiota

transplant, which resulted in resolution of diarrhea, improvement in well being and has kept her out of hospital. Discussion: Clostridium difficile is more prevalent in immunocompromised patients, resulting in significant patient morbidity and strain on health care resources. This novel therapy has the potential to decrease hospitalization rates and length of stay in future especially with early application. To date there are only very few reported cases of the use of this therapy in solid organ transplant patients. 299 POST PARTUM POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME (PRES) SECONDARY TO EPIDURAL ANAESTHESIA R SUD1, S BHASKARA1, G LEE1, M SURANYI1, M DOWLA2, S LIM3, A HENNESSY3, A MAKRIS1,3 1Renal Department, Liverpool Hospital, Sydney, NSW; 2Neurology Methocarbamol Department, Bankstown Hospital, NSW; 3Heart Research Institute, Sydney, Australia Background: Posterior reversible encephalopathy syndrome (PRES) is a neurological disorder that has

been associated with numerous underlying causes. In the post partum period, pre-eclampsia is frequently assumed to be the cause. Case reports of postpartum PRES have been reported due to alternative aetiologies, including spinal anaesthesia. The ratio of soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF) has been shown to discriminate between normal pregnancy and the hypertensive disorders of pregnancy (HDP). These markers may have a role in clarifying causes of post partum PRES. Case Report: We present a case of a 28 year old female presenting with seizures, severe headache, confusion and hypertension 48 hours after a normal vaginal delivery. The delivery was facilitated by an epidural anaesthetic – complicated by dural puncture. Anti-inflammatories were given for perineal pain. MRI findings were consistent with PRES. No proteinuria, liver, renal or haematological abnormalities were demonstrated at presentation. Serum was stored for later measurement of circulating angiogenic markers.

The reasons for these divergent results are still unknown but as we understand more about the immune system in adipose tissue one could speculate several explanations for these discrepancies. One possibility is that microbiome differences between laboratories and between wild-type and knockout mice contribute to the difference in weight gain, as the microbiome has been to shown to significantly impact metabolism GSI-IX purchase and the development of obesity,[65] as well as iNKT cell development.[66] We have exchanged cages between non-littermate wild-type and iNKT knockout mice to reduce the impact of the microbiome. However, the reference standard is to use wild-type and knockout littermates to eliminate

the impact of the microbiome, which were used in some,[63, 67] but not most, of the studies summarized above. Another plausible explanation is the age of mice

in each study. In young mice, there is a substantial population of iNKT cells and fewer regulatory T cells in adipose tissue, and at 8–16 weeks, iNKT cells accumulate further but decline in old age, whereas adipose regulatory T cells greatly accumulate in old mice.[51] Therefore, it is plausible that iNKT cells may be more influential in younger mice, whereas in older mice it is the regulatory T cells that dominate and the role of iNKT cells, or lack of them may be less dominant. It is also possible that for some reason both wild-type and iNKT-deficient animal Dapagliflozin colonies in different laboratories have a more Th1 or more Th2 bias among iNKT cells or other lymphocytes, or in some colonies, there is a compensatory selleck kinase inhibitor mechanism when iNKT cells are absent from birth. Despite the divergent results using iNKT-deficient mice, other methods

to measure the effects of iNKT cells on obesity and metabolism are more consistent. First, over 14 independent studies have shown that iNKT cells (when measured accurately) are depleted in obesity, and all human studies have also found iNKT deficiency associated with obesity. Other immune cells that are shown to be protective in obesity,[52] such as regulatory T cells,[51] alternatively activated macrophages and eosinophils,[54] are depleted in obesity, whereas those that are shown to be pathogenic in obesity like CD8+ T cells[50] and classically activated macrophages[56] are increased in obese adipose tissue. Based on this comparison, which is not direct evidence and merely an association, iNKT cells appear to be part of the protective anti-inflammatory immune cell group that are lost in obesity as an inflammatory response takes over. More direct evidence comes from gain of function experiments, when iNKT cells are adoptively transferred into wild-type or iNKT-deficient obese mice or activated in wild-type obese mice. The majority of studies have shown that this has a positive impact on metabolic control and on protection against weight gain.

In vitro, kinetic analysis of CD1 expression shows that proteins are

detectable over a fairly narrow time range between 2 and 4 days, rather than a highly durable effect (Fig. 3A). Conclusions relating to CD1 expression in the dermis of infected skin can be formally stated for CD1b and CD1c. We also noted an upward trend in CD1a expression, but it did not reach statistical significance (Fig. 1). However, Romidepsin chemical structure large numbers of CD1a expressing LCs in the nearby epidermal compartment provide a higher baseline of staining that complicates interpretation of CD1a expressing cells in the dermis. Collectively, the results show that CD1b and CD1c proteins are rare or absent on cells in the dermis under normal conditions, but are locally upregulated on DCs in the dermis

after coming into the proximity with the infecting borrelial pathogen. Although CD1a selleck induction is linked to CD1b and CD1c in myeloid cells, only CD1a is constitutively expressed at high levels on epidermal LCs. Previous ex vivo studies showed that human dermal DCs and epidermal LCs play distinct roles in response to borrelia infection, with dermal DCs having more efficient mechanisms of internalization and processing of B. burgdorferi25, so it is of interest that the new CD1 appears on the same type of cell that may be most directly exposed to foreign lipid antigens. Triacyl-CSK4 and natural triacylated lipoproteins present in mycobacteria and borrelia bind to hydrophobic pockets in the TLR1-2 heterodimer and signal through Myd88 and NF-κB to stimulate secretion of diverse cytokines 49. The cellular signaling pathway

leading to increased CD1 gene translation might result from cell autonomous signals within TLR-2-expressing cells. However, direct connections between NF-κB signaling and CD1 promoters are not known, and our data show that secreted factors are sufficient to transfer CD1-inducing activity from cell to cell under conditions in which TLR-2 is not activated. These results suggest that the pathogen sets up a local field whereby cytokines stimulate CD1 expression in many cells near the site of infection, even if individual CD1 expressing cells themselves are not infected or in direct Ribonucleotide reductase contact with the pathogen. Although the effects of GM-CSF were known 12, 17, 50, the identification of IL-1β as a regulator of CD1 protein expression provides a new downstream function of this innate cytokine 51. IL-1β has been implicated as an in vitro factor for inducing CD1a expression on LC precursors 52, but identification of mature IL-1β as a group 1 CD1 inducing factor on myeloid cells is a new finding with several implications. First, IL-1β can be used therapeutically as an adjuvant to stimulate CD1 antigen processing function in human monocytes.