That is precisely what Sperling found, even for large arrays of items, as long as the subset to be reported was relatively small (e.g., three to five items). A recent study by Blaser and Kaldy (2010) reported a similar pattern of results in 6-month-old infants. They presented infants with an array Enzalutamide clinical trial of up to 10 items varying in shape and color for a brief 1-sec duration and then highlighted two of the items by removing them from the array for 1/2 sec. When these removed items reappeared, one of them had changed. The dependent measure was whether infants looked at the changed item. As

in Sperling (1960), if all of the items in the array were encoded into STM, then regardless of which subset was highlighted, infants should detect the changed item and look longer at it. However, if infants cannot encode all of the items in the array, there will be a set-size limit beyond which the novelty preference for the changed item will fail to exceed chance. This pattern of results was precisely

what Blaser and Kaldy found—at set sizes of 2, 4, and 6 infants looked longer at the changed item, but at set sizes of 8 and 10 they did not. These results suggest that 6-month-olds have a STM capacity of at least six items in a briefly presented array. Along with prior results on WM, these results also confirm that infants have more limited information-processing capacities than adults, although their capacities are still rather impressive given JQ1 manufacturer the absence of task instructions, motivation, and training. What then mitigates Problem 2—the Methane monooxygenase inability to keep track of all possible statistics? Over the past two decades, a variety of constraints have been proposed and verified experimentally to account for the naïve learner’s ability to overcome the computational explosion problem (i.e., attempting to keep track of everything).

These constraints include the following. Attentional biases—infants appear to “naturally” attend to object shape and to the whole object rather than its parts (Smith, 2003), to syllables rather than phonemes (Bertoncini & Mehler, 1981), to a variety of Gestalt principles (Bhatt & Quinn, 2011) such as proximity, synchrony, and stream segregation (within an octave), and to limit inferences to a single possibility (i.e., mutual exclusivity in object names; Markman, Wasow, & Hansen, 2003). Social cues—infants appear to be guided in their attention by the gaze, manual exploration, and pointing gestures of their caregivers (Baldwin, 1993). Environmental simplification—infants benefit from a variety of ways in which caregivers declutter or enhance stimuli in their proximal environment (Kuhl et al., 1997). Cross-situational statistical learning—infants can determine by a simplified “process of elimination” that names and objects are linked even when these linkages are inferred rather than overt (Smith & Yu, 2008).

Light, corneal, gag, cough and deep tendon reflexes were all lost. There was no electrical activity on EEG.

He died of septic shock secondary to cholecystitis at the age of 32. Serum creatine kinase, lactic acid and pyruvic acid were within normal limits. Other peripheral hematology and blood chemistry were within normal limits. Lysosomal enzymes examined were all in normal ranges. Genetic analysis of SCA8 showed pathogenic CTA/CTG repeat of 23/127 (normal 16–91). Genes for SCA1, 2, 3, 6, 7, dentatorubral-pallidolluysian atrophy (DRPLA) and Huntington’s disease exhibited no pathological expansion. Abnormal fused in sarcoma (FUS) mutation was not confirmed. Thus we clinically diagnosed this case as marked psychomotor impairment, possibly related LY2835219 to the abnormal expansion of SCA8 mutation although other SCA8 cases reported up to now were quite distinct from the present case in clinical features. Autopsy was done 3 h after death. mTOR inhibitor The brain weighed 400 g. Macroscopic examination revealed diffuse atrophy of the whole brain, including the cerebellum,

brain stem and spinal cord. The cerebral cortex and white matter showed atrophy. The basal ganglia, thalamus, cerebellum, tegmentum of the brainstem, midbrain (Fig. 1A), pons, medulla oblongata and spinal cord were severely devastated, obscuring the details of their internal structures. On microscopic examination, the cerebral cortex showed diffuse neuronal loss and Thalidomide gliosis, and white matter atrophy was comparable to that of the gray matter (Fig. 1B). The degrees of neuronal loss and gliosis (graded into mild, moderate to severe) and the frequency of rNCIs are schematized (Fig. 2). Many remaining

neurons had round to oval rNCIs. The frequency of the neurons with rNCIs was variable between 5–30% of remaining neurons. It was low in areas with severe neuronal loss, such as the thalamus, cerebellum (Fig. 1C) and motor nucleus, such as the hypoglossal nucleus (Fig. 1D), while abundant in Ammon’s horn where neuronal cells were spared. It was moderate in the frontal and parietal cortices where neuronal loss was moderate in degree. This inverse relationship between neuronal loss and rNCI was similarly evident by contrasting the deep layers of the cerebral cortex where gliosis was mild with abundant rNCIs. The rNCIs were basophilic on HE (Fig. 3A) and KB (Fig. 3B) and argyrophilic with Bodian silver impregnation (Fig. 3C). The rNCIs were positive: Ub ≈ 25–35% (Fig. 3D, 1:200, Millipore, Tokyo, Japan); p62 ≈ 20–30% (Fig. 3E 1:500, Abnova, Walnut, CA, USA); and phosphorylated TDP43 ≈ 3–5% (Fig. 3F, 1:10 000, Cosmo Bio, Tokyo, Japan), then positive in a few rNCIs for expanded polyglutamine ≈ 0.5–1.0% (Fig. 3G, 1–2, 1:10 000, Millopore, Tokyo, Japan) and negative for Syn (Fig. 3H, 1:10 000, Wako, Tokyo, Japan), AT8 (Fig. 3I, 1:10 000, Innogenetics, Zwijndrecht, Belgium), FUS (Fig. 3J 1:100 gift of Dr Murayama), neurofilaments (Fig.

burgdorferi as it migrates from the tick midgut and salivary glands into mammalian tissue (Schwan et al., 1995; de Silva et al., 1996; Hefty et al., 2001, 2002b). The reciprocal expression of outer surface protein (Osp) A (downregulated) and OspC (upregulated) that occurs during tick feeding was first reported by Schwan and co-workers

in 1995 (Schwan et al., 1995). Subsequent to this seminal report, many laboratories have reported on the identification of several differentially expressed B. burgdorferi antigens, some of which are upregulated by an increase in temperature (Hefty et al., 2001), while others appear to be expressed exclusively during the mammalian phase of infection (Champion et al., 1994; Akins et al., 1995; Suk et al., 1995; Wallich et al., 1995; Fikrig et al., 1999; Hefty et al., 2002b). CP-690550 in vivo Although there are exceptions (Aron et al., 1996), almost all differentially expressed B. burgdorferi antigens identified to date are plasmid encoded Selleckchem ICG-001 (Brooks

et al., 2003; Ojaimi et al., 2003). This has led investigators to speculate that these extrachromosomal plasmid elements are essential for both B. burgdorferi virulence and maintenance of the borrelial enzootic cycle. This notion is further supported by the finding that changes in plasmid content correlate with loss of B. burgdorferi infectivity (Purser & Norris, 2000; Labandeira-Rey & Skare, 2001; McDowell et al., 2001). Prior studies have now shown that many of the borrelial surface antigens are lipid-modified proteins (i.e. lipoproteins). Interestingly, Cox and co-workers noted that several surface-exposed lipoproteins (OspA, OspB, and OspC) are not found exclusively on the surface of the organism. In fact, these lipoproteins can be detected in the periplasm of the organism as well (Cox et al., 1996). Lipoproteins are not only differentially expressed during different stages of the

borrelial enzootic life cycle, but they also can be shuttled to and from the surface of this organism at different points during many infection (Hefty et al., 2002b). The fact that many of the lipoproteins studied to date are located in the periplasm or not surface exposed during mammalian infection precludes specific antibodies from helping to affect clearance of the organism. Therefore, it has become of utmost importance to fully define the expression patterns of candidate surface proteins and fully delineate their cellular location during mammalian infection. At this time, it is not entirely clear how lipoproteins are retained in the periplasm and/or shuttled to the cell surface. While the B. burgdorferi genome encodes the necessary machinery for Sec translocation across the inner membrane (Fraser et al., 1997), it has been proposed that Borrelia may utilize a distinct pathway for lipoprotein transport from the periplasm to the surface of the outer membrane (Schulze & Zuckert, 2006). The genetic makeup of B.

17 Ofsthun et al. reported a similar analysis of 44 550 prevalent haemodialysis patients from the Fresenius Medical Ibrutinib price Care database.18 The relative risk of death for haemoglobin <90 g/L was 2.11 (P < 0.001) compared with a reference haemoglobin level of 110–120 g/L. The relative risk of death decreased to approximately 1.6 and

1.3 as haemoglobin increased to 90–100 g/L and 100–110 g/L, respectively. There was a 16% reduction in mortality for haemoglobin levels between 120 and 130 g/L (RR 0.84, P = 0.007). Fort et al. prospectively studied the effects of time-dependent haemoglobin and ESA dose on mortality in 2310 incident haemodialysis patients from Spain.19 Using a time-dependent multivariate Cox proportional hazard model, the adjusted HR for death was 1.36 (95% CI 1.01–1.86) for a haemoglobin level <100 g/L compared with a level of 111–120 g/L. In contrast, a haemoglobin

level of >130 g/L was associated with a survival benefit (HR 0.69, 95% CI 0.49–0.97). Analysis of the UK Renal Registry data reported similar outcomes with HRs for death for haemoglobin values <100 g/L and >110 g/L being 1.28 (P < 0.001) and 0.64 (P < 0.001), respectively, compared learn more with a reference haemoglobin level of 100–110 g/L.20 The HRs decreased as achieved haemoglobin increased (Hb 110–120 g/L HR 0.63; Hb 120–130 g/L HR 0.47, and Hb >130 g/L HR 0.44). Zhang et al. conducted a retrospective study of 94 569 prevalent patients who were on haemodialysis in 2000 and 2001.21 The patients were divided into quartiles of ESA dose (1388–7905 U/week, 7905–13 377 U/week, 13 377–22 068 U/week and >22 068 U/week) and five categories of

haematocrit values (<30%, 30–33%, 33–36%, 36–39% and >39%). Mortality rates decreased as haematocrit values increased. Within each haematocrit category, mortality rates were lowest in the lowest quartile of ESA dose and highest in the highest quartile. A US Medicare study reported outcomes of 393 967 prevalent haemodialysis patients from 2002 to 2004.22 In a fully adjusted Cox proportional hazard model, mortality was higher at all haematocrit levels Cyclic nucleotide phosphodiesterase below 34.5% compared with the reference haematocrit level of 34.5% to 36%. The HR for death increased from 1.17 (95% CI 1.14–1.20) to 3.11 (95% CI 3.01–3.20) when haematocrit decreased from 33–34.5% to <27%. Similarly, mortality increased at all levels of haematocrit >39%. Mortality was comparable for haematocrit levels between 36% and 39%. When patients were grouped into five categories of erythropoietin dose (0 U/week, 0–6000 U/week, 6000–12 000 U/week, 12 000–18 000 U/week and >18 000 U/week), the HR for death progressively increased with increasing dose of erythropoietin for every level of haematocrit.

[33]. Cells were washed

three times in media and counted. PBMC from cutaneous leishmaniasis patients and non-infected individuals were used for in vitro culture TCR-usage analysis. Cultures were set up using a concentration of 2·5 × 105 cells in 96-well plates in the presence or absence of SLA (10 µg/ml final concentration) and were incubated for approximately 20 h. During the last 4 h of culture, Brefeldin-A (Sigma-Aldrich) (1 µg/ml), which impairs protein secretion by the Golgi complex, was added to the cultures. After the incubation period, cultures were harvested and submitted to flow cytometric analysis to evaluate T cell repertoire, surface markers and cytokine profile. The antibodies used for staining were immunoglobulin fluorescein isothiocyanate (FITC) and phycoerythrin (PE) controls (PharMingen, San find more Diego, CA, USA), anti-Vβ2-biot, anti-Vβ3-biot,

anti-Vβ5·1-biot, anti-Vβ5·2-biot, anti-Vβ11-biot, anti-Vβ17-biot, anti-Vβ 24-biot (Immunotech, Burlingame, CA, USA) anti-Vβ8-FITC, anti-Vβ 12-FITC (Immunotech), SA-FITC (PharMingen), anti-CD69 PE (Ebioscience, San Diego, CA, USA), selleck inhibitor anti-HLA-DR-PE, anti-CD45RO-PE (PharMingen) and anti-CD4-PE-Cy5 (Ebioscience). The anti-cytokines antibodies used were PE-labelled anti-IFN-γ, anti-TNF-α (PharMingen) and anti-IL-10 (Caltag, Carlsbad, CA, USA). PBMC were analysed for their repertoire, surface markers and intracellular cytokine expression pattern. Briefly, 2·5 × 105 PBMC were cultured in 96-well plates in

200 µl cultures for 20 h with either media alone or SLA (at 10 µg/ml final concentration). Brefeldin-A (1 µg/ml) was added during the last 4 h of culture to impair protein secretion, allowing for cytokine intracellular staining, as performed previously by us [11]. The cells were then stained for T cell receptor Vβ repertoire and surface markers, and fixed using 4% formaldehyde (Sigma-Aldrich). Cells were then permeabilized with a solution of saponin (Sigma-Aldrich) and stained, for 30 min at 4°C, using anti-cytokine monoclonal antibodies directly medroxyprogesterone conjugated with PE. PE-labelled immunoglobulin control antibodies and a control of unstimulated PBMC were included in all experiments. Preparations were washed and fixed as described in the previous section and analysed using fluorescence activated cell sorter analysis (FACS), selecting the total lymphocyte population (Fig. 1). In all cases both cytokine and surface marker staining were associated with T cell receptor Vβ repertoire staining for studying the expression of cytokines and surface markers together and the phenotype of the cells that produced them. At least 40 000 gated events were acquired for later analysis.

A summary of the IFN-γ analysis is shown in Table 1. Two weeks after final vaccination a statistically significant increase of IFN-γ secretion

by ADV-stimulated PBMC was observed in all vaccinated groups of animals compared with unstimulated control. The level of IFN-γ produced by PBMC obtained from previously vaccinated pigs after stimulation with ADV was at least 14-fold click here higher than the mean IFN-γ basal production (unstimulated PBMC) and was at least 110 pg mL−1. The significantly higher concentration of IFN-γ was noted especially in group 2 (vaccinated at 10 and 14 weeks), where it reached 448 ng mL−1 (60-fold higher than basal production). In the next sampling period, at 20 weeks of life, the amounts of IFN-γ in supernatant were higher than 110 pg mL−1 only in groups 2 (vaccinated at 10 and 14 weeks), 4 (vaccinated at 12 weeks) and 6 (vaccinated at 1 and 12 weeks). These results are in agreement with data observed in the proliferation assay. In groups 3 and 5 (vaccinated at 1 week and at 1 and 8 weeks of age, respectively) the concentration of IFN-γ was only six- and twofold higher than in the mean basal secretion and reached 50 and 30 pg mL−1, respectively, whereas in the remaining vaccinated groups the level of this cytokine was still high

(at least 17 times higher than in unstimulated control). In the unvaccinated group (group 1) there was no significant increase of IFN-γ concentration after ADV stimulation in any sampling period. Dabrafenib The highest concentration of investigated cytokine in culture supernatants was observed in group 2 (vaccinated at 10 and 14 weeks of age). There was a positive correlation between IFN-γin vitro production and proliferation response of PBMC stimulated with ADV (r=0.6, P≤0.05). In vitro ADV stimulation did not induce production of IL-4 by PBMC in either immune or nonimmune pigs. In supernatants from stimulated and unstimulated

cultures the level of IL-4 was undetectable (<15.6 pg mL−1). Aujeszky's disease is still a significant infectious disease in Poland and vaccination of animals is an important element of AD eradication. As a result, many animals possess MDA, which may disturb the immune GNA12 response to vaccine antigen. The amount of passively acquired antibodies transmitted to a given piglet depends on several factors: colostral intake, number of suckling piglets and antibody titers of sows (Andries et al., 1978). In the present study the level of MDA against gB antigen was high and similar in piglets from all six groups. Lack of specific T-cell response in 40% animals vaccinated once in the presence of a relatively high level of MDA (group 3, vaccinated at 8 weeks of age) may suggest that MDA suppresses not only humoral but also T-CMI and that for development of cellular immunity in 100% of vaccinated animals in the presence of MDA a single dose of vaccine was insufficient.

While there is a great deal that we do not understand about the biology of HIV transmission, we do know biological factors are critical determinants of exposure outcome.21,22 The most important determinants of transmission are (i) the HIV level in the blood and genital/rectal secretions of the HIV-infected partner and (ii) the number and density

of HIV-susceptible target cells to which the virus can gain access at the site of exposure (usually the mucosal lining of the penis, rectum or female genital tract) in the HIV-uninfected partner.23,24 As will be discussed, these two critical determinants are affected by numerous, overlapping biological factors: we hypothesize that this biology, in addition to any sociocultural and economic factors, has played and continues to play an important role in the racial imbalance that characterizes the global HIV pandemic. Important biological factors and the potential interactions of these factors with race Nivolumab and geography are now reviewed under the broad headings of viral factors, host genetic factors, co-infections and host immunology. HIV-1 group M viruses are subdivided into several subtypes or clades based on genetic heterogeneity: these clades have strong geographical associations,25

and considerable research has examined the potential associations of clade with HIV transmission. Clade C predominates globally and is responsible for most HIV infections in southern Africa and India, while clade B predominates in North America, Europe and Australia. East Africa is dominated Erlotinib by clade A and to a lesser extent D, while the recombinant virus designated CRF01_AE (previously clade L-gulonolactone oxidase E) is most common in Thailand. Early studies suggested that clade C and CRF01_AE were more easily transmitted through heterosexual sex,26 potentially because they bound preferentially to Langerhans cells in the vaginal mucosa and penis.27 Research continues in this area, and more recent work has found that HIV clade C shows enhanced replication (compared to clade A) in a dual virus culture system, as well as in an ex vivo cervical explant model;28

in addition, observational studies demonstrate that clade A may be transmitted more easily than clade D.29 While these data are interesting, it is probably fair to say that it remains unclear what effect, if any, virus clade has on patterns of HIV epidemic spread in the real world. Certainly, virus subtype cannot explain racial differences in HIV prevalence that are apparent in multiple regions and across different virus clades. The clearest association of viral factors with HIV transmission is the plasma HIV RNA viral load, with higher plasma levels being associated with stepwise increases in the probability of transmission30 and in virus levels within genital secretions.21 There are a few data to suggest that plasma viral load varies substantially with viral clade, geography or race per se.

Here, we identified allograft inflammatory factor 1 (AIF1, Iba1) and sialic acid binding Ig-like lectin 1 (SIGLEC1) as putative NHD-specific biomarkers by bioinformatics analysis of microarray

data of NHD DC. We studied three NHD and eight control brains by immunohistochemistry with a panel of 16 antibodies, including those against Iba1 and SIGLEC1. We verified the absence of DAP12 expression in NHD brains and the expression of DAP12 immunoreactivity selleckchem on ramified microglia in control brains. Unexpectedly, TREM2 was not expressed on microglia but expressed on a small subset of intravascular monocytes/macrophages in control and NHD brains. In the cortex of NHD brains, we identified accumulation of numerous Iba1-positive microglia to an extent similar to control brains, while SIGLEC1 was undetectable on microglia in all the brains examined. These observations indicate that human

microglia in brain tissues click here do not express TREM2 and DAP12-deficient microglia are preserved in NHD brains, suggesting that the loss of DAP2/TREM2 function in microglia might not be primarily responsible for the neuropathological phenotype of NHD. “
“Glucose transporter-1 (GLUT-1) is one of the major isoforms of the family of glucose transporter proteins that facilitates the import of glucose in human cells to fuel anaerobic metabolism. The present study was meant to determine the extent of the anaerobic/hypoxic state of the intratumoral microenvironment by staining for GLUT-1 in intracranial non-embolized typical (WHO grade I; n = 40), brain invasive and atypical (each WHO grade II; n = 38) and anaplastic meningiomas (WHO grade III, n = 6). In addition, GLUT-1 staining levels were compared

with the various histological criteria used for diagnosing WHO grade II and III meningiomas, namely, brain invasion, increased mitotic activity and atypical cytoarchitectural change, defined by the presence of at least three out of hypercellularity, sheet-like growth, prominent Mirabegron nucleoli, small cell change and “spontaneous” necrosis. The level of tumor hypoxia was assessed by converting the extent and intensity of the stainings by multiplication in an immunoreactive score (IRS) and statistically evaluated. The results were as follows. (1) While GLUT-1 expression was found to be mainly weak in WHO grade I meningiomas (IRS = 1–4) and to be consistently strong in WHO grade III meningiomas (IRS = 6–12), in WHO grade II meningiomas GLUT-1 expression was variable (IRS = 1–9). (2) Histologically typical, but brain invasive meningiomas (WHO grade II) showed no or similarly low levels of GLUT-1 expression as observed in WHO grade I meningiomas (IRS = 0–4).

Cultured B-1 cells selleck kinase inhibitor were stained with PE-labelled anti-CD138 antibody (clone 281-2) (all antibodies from BD Pharmingen). For assessment of proliferation, freshly isolated B-1 cells were stained with 2 μmol/l CellTrace™ CFSE (Invitrogen), according to the manufacturer’s protocol, before the experiment. At the end of

the experiment, cells were harvested and directly resuspended for analysis. For apoptosis assays, cultured B-1 cells were stained with FITC-labelled annexin V (FITC annexin V apoptosis detection kit; BD Pharmingen) and cell viability solution containing PI3K inhibitor 7-aminoactinomycin D (7-AAD) (BD Pharmingen),

according to the manufacturer’s instructions. Cells were analysed using a FACS Aria II (BD Pharmingen) and at least 100 000 cells were counted per sample in in-vivo experiments and at least 5000 cells in in-vitro experiments, with dead cells excluded based on FSC. Specific IgM and IgG antibodies were determined in plasma and in cell culture supernatants by chemiluminescent ELISA, as described previously [7]. For detection of total IgM, microtitre plates were coated with purified rat anti-mouse IgM (2 mg/l) (clone II/41; BD Pharmingen). For the analysis of specific

IgMs, microtitre plates were coated with copper oxidized (CuOx)-LDL (5 mg/l), MDA-LDL (5 mg/l) or Pneumovax CHIR-99021 solubility dmso (10 mg/l). CuOx-LDL and MDA-LDL were prepared from human LDL, as described previously [25]. Plates were post-coated with Tris-buffered saline (TBS) containing 1% bovine serum albumin (BSA) and samples were incubated for 1 h. Serum samples were diluted in TBS containing 1% BSA to a final dilution of 1:300 for detection of total IgM, 1:100 for IgM against CuOx-LDL and MDA-LDL and 1:50 for IgM against Pneumovax. Cell culture supernatants were diluted 1:125 for detection of total IgM and IgM against CuOx-LDL and MDA-LDL. Antibodies in samples were detected with alkaline phosphatase-conjugated goat anti-mouse IgM (μ-chain specific; Sigma-Aldrich) and quantified with Lumiphos 530 (Lumigen, Inc., Southfield, MI, USA) using LMaxII (Molecular Devices, Sunnyvale, CA, USA). Total RNA from isolated peritoneal B-1 cells and positive control tissue (mouse liver, skeletal muscle and placenta) was extracted with the RNeasy micro prep kit (Qiagen, Hilden, Germany), according to the manufacturer’s instructions.

They are made available as submitted by the authors. “
“6-Sulpho LacNAc dendritic cells (slanDC) are a major population of human blood DC that are highly pro-inflammatory, as characterized by their outstanding

RAD001 chemical structure capacity to produce tumour necrosis factor-α and interleukin-12 (IL-12) and to prime antigen-specific T-cell responses. SlanDC were found to be present in inflamed tissue such as atopic dermatitis, where high levels of histamine are also present. As histamine is an important regulator of allergic inflammation we investigated the role of histamine receptors, particularly the most recently identified histamine H4 receptor (H4R), in modulating the pro-inflammatory function of slanDC. The expression of H4R was evaluated by real-time PCR and flow cytometry. Cytokine production in response to H4R stimulation was assessed by intracellular flow cytometric staining and enzyme-linked immunosorbent assay. We show that slanDC express the H1R, H2R and H4R on mRNA and the H4R on protein level. No differences were observed in basal H4R expression in patients with atopic dermatitis and psoriasis, but in Pifithrin-�� order atopic dermatitis

patients the H4R was up-regulated by interferon-γ. When stimulated with lipopolysaccharide in the presence of histamine, slanDC produced substantially lower levels of the pro-inflammatory cytokines tumour necrosis factor-α and IL-12, mediated solely via the H4R and via the combined action of H2R and H4R, respectively. In contrast, the production of IL-10 was not affected by histamine receptor

activation on slanDC. 2-hydroxyphytanoyl-CoA lyase The slanDC express the H4R and its stimulation leads to reduced pro-inflammatory capacity of slanDC. Hence, H4R agonists might have therapeutic potential to down-regulate immune reactions, e.g. in allergic inflammatory skin diseases. 6-Sulpho LacNAc expressing dendritic cells (slanDC) were previously identified as a new subset of human DC.1 SlanDC account for 0·5–2% of the peripheral blood mononuclear cells (PBMC) and therefore represent the largest population of DC present in human blood. SlanDC appear as important pro-inflammatory immune cells because they show great capacity to induce primary antigen-specific T-cell responses2 and they up-regulate the expression of the activation marker CD69 and the secretion of IFN-γ (interferon-γ) in natural killer cells.3 Moreover slanDC stand out by their high-level production of tumour necrosis factor-α (TNF-α) and they are the main source of interleukin-12 (IL-12) among blood leucocytes compared with monocytes and CD1c+ DC.4 In contrast to classical CD1c+ DC and plasmacytoid DC, slanDC express anaphylatoxin receptors (C5aR, C3aR) and were shown to migrate in response to C5a stimulation in vivo.5 In T helper type 1 (Th1) -mediated diseases slanDC were shown to infiltrate the inflamed tissue: they have been identified in the dermis of patients suffering from psoriasis vulgaris and in the pannus tissue of rheumatoid arthritis.