For all subsequent statistical analyses, IL-8, TNFα and IL-10 concentrations present in un-stimulated cultures were subtracted to give stimulus-specific cytokine levels for each

individual. The ratio of IL-10: TNFα was calculated from stimulus-specific cytokine levels. As cytokine concentrations, IL-10: TNFα ratios, smp0–3 h RP: m0–3 h RP cytokine ratios, and leucocyte percentages did not meet parametric assumptions, the Mann–Whitney U-test and Kruskal–Wallis tests were used to compare between two independent groups and K independent groups, respectively. The Wilcoxon signed-rank LY2835219 cell line test was used for paired comparison of periodate-treated and mock-treated WB culture cytokine production. This study comprised a total of 47 individuals from the Diokhor Tack community aged 6–53 years old, of whom 13 were not infected, 14 infected with S. mansoni only and 20 co-infected with S. mansoni and S. haematobium (Table 1). Only two participants

in the co-infected group were also positive for soil-transmitted nematode eggs. S. mansoni infection intensity did not significantly differ according to gender (F1,30: 1·433, P = 0·241), age group (F1,30: 1·397, P = 0·246) or between infected and co-infected groups (F1,30: 2·380, P = 0·133). S. haematobium infection intensity also did not significantly differ between males and females (F1, 17: 0·240, P = 0·631) selleck chemicals or between age groups (F3,17: 2·501, P = 0·132) in the co-infected group. To investigate innate/early immune responses to 0–3 h RP, IL-8, TNFα and IL-10 were quantified in Farnesyltransferase whole-blood supernatants 24 h post-stimulation. Levels of all three cytokines were significantly higher in 0–3 h RP-stimulated cultures than in un-stimulated cultures (IL-8 Z: −5·968, P < 0·001; TNFα Z: −5·905, P < 0·001; IL-10 Z: −5·968, P < 0·001) with

all 47 participants mounting a detectable cytokine response to 0–3 h RP. Participants also produced higher levels of IL-8, TNFα and IL-10 in response to zymosan than in un-stimulated control cultures (IL-8 Z: −5·968, P < 0·001; TNFα Z: −5·841, P < 0·001; IL-10 Z: −5·905, P < 0·001). Interestingly, stimulus-specific IL-8 and IL-10 levels were higher in response to 0–3 h RP than to an equivalent concentration of zymosan in paired cultures (Wilcoxon signed-rank test, IL-8 Z: −5·661, P < 0·001 and IL-10 Z: −4·370, P < 0·001), whilst TNFα levels were higher in response to zymosan than to 0–3 h RP (Wilcoxon signed-rank test, Z: −4·529, P < 0·001). There was no significant correlation between levels of any of the 0–3 h RP-specific cytokines, and schistosome infection intensity and levels did not differ between age groups (data not shown).

“
“Teratomas are very rare intracranial tumors and cytogenetic information on this group remains rare. We report a case of a mature teratoma with abnormal +21 trisomy Tanespimycin mouse in tumor karyotype ocurring in a non-Down syndrome (DS) infant. Additionally, the evidence for the contribution of chromosome 21

trisomy in this neoplasia are briefly reviewed. The 6-month-old male baby presented with a posterior fossa tumor. Histological evaluation of tumor specimen showed a mature teratoma composed of fully differentiated ectodermal, mesodermal and endodermal components. Although somatic karyotyping of the index case was normal, composite tumor karyotype depicted 47, XY, +21[6]/46,XY[6]. Besides previous reports of children with DS and intracranial teratomas, this is the first report to describe the occurrence of an isolated chromosome 21 trisomy within the tumor of a non-DS child. The participation of chromosome 21 in this rare pediatric tumor, either somatic or restricted to tumor specimen, may deserve special interest and further investigation. “
“Innate immunity within the central nervous system (CNS) is primarily provided by resident microglia. Microglia are pivotal in immune surveillance and also facilitate the co-ordinated responses

between the immune system and the brain. For example, microglia interpret and propagate inflammatory signals Dorsomorphin purchase that Resveratrol are initiated in the periphery. This transient microglial activation helps mount the appropriate physiological and behavioural response following peripheral

infection. With normal ageing, however, microglia develop a more inflammatory phenotype. For instance, in several models of ageing there are increased pro-inflammatory cytokines in the brain and increased expression of inflammatory receptors on microglia. This increased inflammatory status of microglia with ageing is referred to as primed, reactive or sensitized. A modest increase in the inflammatory profile of the CNS and altered microglial function in ageing has behavioural and cognitive consequences. Nonetheless, there are major differences in microglial biology between young and old age when the immune system is challenged and microglia are activated. In this context, microglial activation is amplified and prolonged in the aged brain compared with adults. The cause of this amplified microglial activation may be related to impairments in several key regulatory systems with age that make it more difficult to resolve microglial activation. The consequences of impaired regulation and microglial hyper-activation following immune challenge are exaggerated neuroinflammation, sickness behaviour, depressive-like behaviour and cognitive deficits.

Stocks of MCMV, Smith strain and mutant MCMV lacking m157 (△m157) 34 were produced in cell culture using B6 mouse embryo fibroblasts or by serial passage of salivary gland homogenates in BALB/c mice in vivo. Tissue culture-derived MCMV was used for inducing T-cell responses and salivary gland virus (SGV) for NK-cell studies. Mice were infected i.v. with 200 PFU LCMV-WE, 2×106 PFU VSVIND, 2×106 PFU VV, 2×106 PFU tissue culture-derived MCMV

(i.p.), 5×105 PFU tissue culture-derived Δm157 MCMV (i.v.) or 5×104 PFU SGV MCMV (i.p.). Cells (105–106 in 50–100 μL) were stained with appropriately diluted mAb (0.1–1 μg in 50–100 μL) in PBS containing 2% FBS and 0.1% NaN3 at 4°C for 30 min. The following fluorescence-labeled mAb were purchased from BD Pharmingen and eBioscience (NatuTec GmbH, Frankfurt, Germany): anti-CD3, -CD5, -CD8, -CD11b, -CD27, -CD62L, -CD127, AZD1208 price -NK1.1. Anti-KLRG1 mAb (clone 2F1) 20 was produced in cell culture, purified using protein G and labeled with Alexa488 or Alexa647 (Molecular probes,

Invitrogen, Karlsruhe, Germany). LCMV- and VSV-specific CD8+ T cells were detected Daporinad clinical trial using PE-labeled H-2Db tetramers complexed with GP33 peptide (KAVYNFATM) and H-2Kb tetramers complexed with NP52 peptide (RGYVYQGL) generated in the laboratory as described 12. Samples were analyzed by a BD FACSCalibur flow cytometer (BD Biosciences) using CellQuest-Pro software (BD Biosciences). Spleen cells (105 in 200 μL) were stimulated for 5 h in 10 μg/mL brefeldin A with 10−6 M of the following peptides: LCMV GP33–41 (KAVYNFATM), MCMV M45985–993 (HGIRNASFI), MCMV M38316–323 (SSPPMFRV), MCMV m139419–426 (TVYGFCLL). Intracellular cytokine staining was performed with PE-labeled mAb specific for IFN-γ (XMG1.2, Loperamide eBioscience) and IL-2 (JES6-5H4, eBioscience)

using Cytofix/Cytoperm solution (BD PharMingen). Peptides were purchased from Neosystem (Straßburg, France). P14 chimeric mice were generated by adoptive transfer (i.v.) of 105 P14 T cells from P14 KLRG1 KO or P14 WT mice. Repetitive P14 T cell transfers to generate 1°, 2° and 3° memory P14 cells were performed as described 11. Memory P14 T cells used for repetitive adoptive transfers were purified using PE-labeled anti-Thy1.1 mAb and anti-PE MACS-MicroBeads (Milteny, Bergisch Gladbach). NK cells were activated in vivo by i.v. injection of VSVIND (2×106 PFU), VV (2×106 PFU), L. monocytogenes (106 CFU), LCMV (200 PFU) or 5×104 PFU MCMV (SVG) i.p. After 20 h, spleen cells were analyzed by staining with CD3-, CD11b-, CD27- and NK1.1-specific mAb. The activity of poly(I:C)-activated NK cells (200 μg i.p., 18 h) was determined by intracellular IFN-γ staining using plate-bound stimulation with anti-NK1.1 mAb (10 μg/mL) in the presence of 10 μg/mL brefeldin A or by classical 4 h 51Cr release assays using RMA-S target cells.

Our immunocytochemical data confirmed that the greatest majority of CD4+ CD25+ cells were Foxp3+ (Fig. 3b). Furthermore, we performed Foxp3 staining on cytospin preparations of the CD4+ CD25−

fraction as well. Foxp3-positive cells were observed in this fraction in agreement with our flow cytometric data (Fig. 3b). In conclusion, the immunocytochemical stainings of the cytospin preparations confirmed that, indeed, there is a CD4+ CD25− cell population that expresses Foxp3 in human normal early pregnancy decidua. Finding the presence of CD4+ CD25− Foxp3+ cells in decidua, we wanted to clarify whether these cells belonged to the Treg phenotype or whether they were conventional Th cells. It has been shown that small amounts of Foxp3 could be present in conventional Selleckchem Raf inhibitor effector cells, while naïve Treg- precursor cells express higher and steady state Foxp3.38

Accordingly, we analyzed the relative expression of Foxp3 mRNA in CD4+ CD25− Foxp3+ and CD4+ CD25+ Foxp3+ cell subsets isolated from 10 consecutive decidual and PBMC samples from first trimester normal pregnancies. The results are summarized in Fig. 4. As can be seen, the expression of Foxp3 mRNA in the CD4+ CD25− subpopulation was comparable to that of the CD4+ CD25+ subpopulation while the expression of TGFβ mRNA was very low. In addition to TGFβ1, we evaluated the mRNA expression in these cells for a panel of 14 cytokines: IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-13, IL-15, IL-17, TNFα, IFN-γ, GM-CSF, and TGFβ1, designed to discriminate between Th1, Th2, Th17, Thiamet G and the regulatory Th3 and Tr1 cytokine profiles. The results are summarized CH5424802 clinical trial in Table I where the cytokine profile of the CD4+ CD25− cells from each individual decidual sample is presented (n = 10). As can be seen, the CD4+ CD25− cells in 4 of 10 samples had a cytokine

profile similar to Th3, although with a low expression of TGFβ1. In fact, the general impression from this analysis was that rather few cytokines were expressed in the CD4+ CD25− samples (Table I). In contrast, the CD4+ CD25− cells in the peripheral blood of pregnant and non-pregnant women showed a very low expression of both Foxp3 and TGFβ mRNA compared with the decidual CD4+ CD25− Foxp3+ and circulating CD4+ CD25+ Foxp3+ Treg cells suggesting that they are another, non-regulatory T-cell subset, e.g. T effector cells (Fig. 4). Summarizing these results, we can conclude that: (i) the majority of the decidual CD4+ CD25− Foxp3+ cell subset, with a stable and comparable Foxp3 mRNA expression and a very low TGFβ mRNA expression, might be Treg cell precursors that have not yet acquired production of the immunosuppressive TGFβ, however, we cannot exclude that some of these cells are CD4+ activated effector cells; and (ii) the naïve CD4+ CD25− Foxp3+ Treg cells were absent in the periphery, suggesting that they are produced in the decidua and might be a reservoir for a local maturation of decidual CD4+ CD25+Foxp3+ Treg cells.

Interestingly, in our study, IFN-γ also appeared to play a regulatory role. It is generally accepted that IFN-γ is produced by Th1 cells and favour the production of IgG1 and IgG3 opsonizing and complement-fixing antibodies, thus, being very useful for the protection against intracellular parasites (41,42). However, recent research indicates that during the acute phases of the infection, viral epitope-specific Treg cells express

both IL-10 and IFN-γ to suppress effector cell proliferation GS-1101 in vitro (43). Furthermore, IFN-γ exerts regulatory functions to limit tissue damage associated with inflammation and to modulate Th and regulatory T-cell differentiation (44). Thus, the emerging concept of regulatory T-cell diversity and polarization has shed light on the controversial issue of IFN-γ involvement in regulatory T-cell development (45). Many researchers have documented that IFN-γ-mediated responses that have protective effects on S. japonicum infection are observed in early phase of schistosome infection (46,47). Nevertheless, numerous studies have suggested that IFN-γ promotes the development and differentiation of regulatory T cells, which can negatively regulate immune response in specific conditions (48,49). These findings suggest that IFN-γ can have paradoxical functions in a context- and disease-specific manner. Our results demonstrated that rSj16 could induce a

special subset of Epigenetics inhibitor Tregs that express IFN-γ and IL-10. This might have a potential role to prevent excessive inflammation and subsequent organ damage. Also, future studies are required to focus on its mechanism during infection with S. japonicum. T-bet is a master regulator for Th1-cell differentiation and also up-regulated through IFN-γ-STAT1 signalling in Foxp3+ regulatory T cells. Meghan A. Koch et al. (50) reported that in response to IFN-γ, regulatory T cells can up-regulated the T helper 1(Th)-specifying transcription factor (T-bet) that promotes the expression of Avelestat (AZD9668) the chemokine receptor CXCR3 on regulatory T cells. Thus, T-bet+ regulatory T cells could accumulate

at sites of Th1-mediated inflammation, and Foxp3+T-bet+ cells represent a novel subset of regulatory T cells that selectively dampen Th1 cell responses (50); therefore, such a differentiation constitutes a negative feedback loop that contributes to the homoeostatic action of IFN-γ (50). In our experiments, as expected, there was an increased expression of T-bet in rSj16-induced regulatory T cells, but not in SEA-induced regulatory T cells. At least in an aspect of IFN-γ production, there was obvious difference between rSj16-induced regulatory T cells and SEA-induced regulatory T cells. It is conceivable that rSj16-induced regulatory T cells may work in concert to achieve sufficient immune regulation that is ultimately beneficial for cercariae penetrating into the skin.

Mast cells are activated by antigen crosslinking of IgE-bound high-affinity receptor for IgE (FcεRI) receptors, and aggregation of these receptors results in rapid phosphorylation of tyrosine residues in the ITAMs of β and γ chains by lyn kinase, which leads to recruitment and activation of spleen tyrosine kinase (syk) and fyn. selleck products Both fyn and syk phosphorylate downstream targets, leading to calcium mobilization,

degranulation, arachidonic acid metabolization, and cytokine and chemokine gene transcription 9, 10. As opposed to activation, desensitization is a process in which mast cells are rendered hypo-responsive to an activating challenge, either by exposure to low antigen doses in calcium-depleted conditions 11 or by exposure to incremental

doses of antigen, in the presence of calcium 12, 13. Calcium-depleted conditions cannot be applied to human desensitizations, and few studies have addressed physiological desensitizations, since events occurring in the absence of extracellular calcium may not reflect the same pathways PF-01367338 manufacturer as those occurring in the presence of calcium 14. Internalization of FcεRI through progressive crosslinking at low levels of antigen has been postulated as the likely mechanism for cell-surface depletion of IgE and cellular unresponsiveness to specific activating doses of allergen 12. Depletion of molecular targets of activation such as syk has been shown in prolonged antigen desensitization, indicating a universal rather than specific desensitization 15. Based on our previous study 16, we report here a model of mouse BM-derived mast cell (BMMCs) specific rapid desensitization to DNP and OVA antigens in the presence of physiologic levels of calcium. Increasing doses of antigen delivered at fixed time intervals induced a highly specific and prolonged hypo-responsiveness to triggering doses of the desensitizing antigen.

Mast cells desensitized to DNP or OVA demonstrated almost complete inhibition of β-hexosaminidase and pre-formed TNF-α release, calcium flux and arachidonic acid metabolization. They did not release significant amounts of newly generated IL-6 or TNF-α and failed to phosphorylate STAT6 and p38 MAPK. When sensitized to both DNP and OVA antigens, DNP-desensitized cells responded fully to OVA and vice versa. Most importantly, Diflunisal specific rapid desensitization targeted the internalization of antigen/IgE/FcεRI complexes since antigen-specific IgE bound to the α chain of the FcεRI remained at the membrane level. This model may provide support for the specificity and effectiveness of human desensitizations. In order to compare single-dose antigen delivery (activation) with sequential cumulative doses (rapid desensitization), we first assessed the dose response curve to DNP-human serum albumin conjugated (DNP-HSA) antigen, by β-hexosaminidase release, with cells sensitized with anti-DNP IgE (see Fig. 1A).

Mutations within a viral genome often confer advantages in vivo, the evolution of which is driven strongly by immune selection pressures. Immune control of the virus before it is able

to mutate is therefore crucial in determining long-term outcome to infection (see Fig. 5). see more In HIV and simian immunodeficiency virus (SIV), viral escape mutations within immunodominant epitopes play a critical role in early and late loss of immune control [50–52] and this is also shown to influence long-term outcome in acute HCV infection [53,54]. There is a variation in the degree of escape between different epitopes within the viral genome of such persistent viral infections, where some epitopes are observed to escape while others are often conserved. One explanation which has been proposed for this is that more sensitive T cells are associated with escape (‘driver’ responses), while Idasanutlin less sensitive cells may be simply ‘passengers’ which have little impact on viral evolution or disease outcome [55]. More sensitive populations are observed to drive viral escape, whereas less sensitive CTLs are associated with epitope stability in both HCV [56] and SIV [57]. In HIV, CTL responses

to the promiscuous epitope TL9-Gag were compared between HLA types within the B7 supertype. B*8101-restricted TL9-Gag responses were found to be of significantly higher functional sensitivity than those restricted by B*4201. Higher TL9-Gag sequence variation is observed in B*8101 compared to B*4201-positive

patients [58]. There is a clear conflict of interest in the outcome of better-quality CTL responses. The immune advantages of improved clearance of the more sensitive responses would appear to be balanced against the disadvantage of driving evolution of the virus in its ability to escape the host immune response. However, viral fitness costs associated with the acquisition of escape mutations may contribute to the protective nature of some HLA class I alleles, such as B57 [3]. CTL dysfunction is seen in a number (-)-p-Bromotetramisole Oxalate of chronic viral infections in humans [59,60] and animal models [61,62]. The genesis of such dysfunction is not well understood, but is thought to be related to repetitive triggering through the TCR. One possible outcome is that more sensitive cells might become preferentially over-stimulated and anergic in the presence of high antigen load. This is supported by in vivo studies showing the persistence of anergic CTLs with high functional sensitivity under such conditions [63,64]. The distinct sensitivities observed in cells of the acute and chronic phase of HIV-1 appears to be a consequence of deletion of the more sensitive cells, as determined by clonotypic analysis of TCR VB chains by polymerase chain reaction (PCR).

They were examined at 0, 1, 3, 6 and 12 months. The factors influencing the prognosis were investigated. The stone discharge was monitored by ultrasonography. Overt renal and liver damage and underlying renal injury markers were analyzed. Results:  The stone discharge rates 1, 3, 6 and 12 months after the diagnoses were 52.5%, 67.2%, 88.3% and 95.5%, respectively. Stone size was a stable influencing factor for the stone discharge rate.

Additionally, the values of the potential renal injury markers in children with stones already discharged is find more equivalent to normal children. Conclusion:  This 12 month follow up of early renal injury markers indicated that the damage to the kidney is temporary with no persistent negative outcomes being found till now. Additionally, the gross development of the children seemed not yet jeopardized by melamine. Longer-term follow up will be conducted. “
“To investigate the potential effects of berberine on renal interstitial fibrosis (RIF) of obstructed kidneys in a unilateral ureteral obstruction (UUO) rat model. Forty-eight rats were randomly divided into three groups: sham-operated, vehicle-treated UUO, and berberine-treated UUO. Rats were gavaged with berberine (200 mg/kg per day) or vehicle. Eight randomly chosen rats in each group were kiled and specimens were collected at day 14 after UUO. Physiological

parameters click here and histological changes were assessed, RIF was evaluated using Masson’s trichrome and Sirius red staining, oxidative stress and inflammation markers were determined, transforming growth factor β1 (TGF-β1), phosphorylated Smad3 (pSmad3) and α-smooth muscle actin (α-SMA)

were measured using immunohistochemistry or western blotting analysis. The obstruction was relieved at day 14 by percutaneous nephrostomy in the remaining UUO rats. The resistive index of left kidneys was undertaken by coloured Doppler flow imaging at day 14 before nephrostomy and day 7 after the 6-phosphogluconolactonase relief. Berberine treatment significantly attenuated RIF induced by UUO. The UUO-induced reduction in kidney superoxide dismutase and catalase activities increased, whereas elevated kidney malondialdehyde level markedly decreased. Berberine treatment significantly ameliorated UUO-induced inflammation, and decreased TGF-β1, pSmad3 and α-SMA expression of UUO kidneys. Moreover, berberine treatment significantly suppressed the increase of resistive index compared with UUO group at day 14 after UUO as well as day 7 after the relief of obstruction. Berberine treatment ameliorates RIF in a UUO rat model by inhibition of oxidative stress, inflammatory responses, and TGF-β1/pSmad3 signalling. “
“Observational reports suggest extended dialysis hours are associated with improved outcomes. These findings are confounded by better prognostic characteristics among people practising extended hours.

Soaking protocols were successfully applied in nematode parasites belonging to clade III [A. suum, O. volvulus, B. malayi and L. sigmodontis (111–116)] and improved for specificity and efficiency to reduce off-target effects, toxicity and costs. In contrast, successful RNAi in

worms of clade V has only been reported for a small percentage of genes that were investigated in this group of nematodes [for example (117)]. Silencing effects on different genes from T. colubriformis, H. contortus and O. ostertagi were often inefficient, difficult to reproduce and dependent PFT�� supplier on delivery method used (118–121). In a more recent study, Lendner and colleagues failed to establish knock-down of tropomyosin in various life stages of H. polygyrus. PF-6463922 In this study, dsRNA seemed not to be taken up efficiently by the parasite regardless of delivery by feeding, soaking or electroporation, with the latter even found to be lethal to L1 larvae (122). As most described techniques for dsRNA delivery involve the removal of the parasite from the host, one major obstacle for successful RNAi is the ability to maintain healthy, viable worms under in vitro culture conditions required for consistent silencing effects (123). Therefore, RNAi approaches are limited to certain life stages of the respective parasite. To circumvent difficulties associated with common RNA delivery techniques, Song et al. tested

a new approach to establish RNAi in B. malayi parasites targeting

genes in developing larvae within the intermediate host. Aedes aegypti mosquitoes were injected with dsRNA or siRNA targeting the B. malayi cathepsin L-like protease. Supplying the RNAi trigger in vivo to healthy worms in a host environment (‘in squito’) led to the highest reported specific reduction in target gene expression in B. malayi (83%) resulting in multiple phenotypes (124). These included reduced motility (69%) and growth retardation (48%) that lead to the prevention of larval development and reduced numbers of larvae migrating to the head of the mosquito, thereby abolishing parasite Glutamate dehydrogenase transmission, decreasing parasite burden and increasing host survival. The mechanism by which the siRNAs reach the parasite within the mosquito is unclear but rapid dissemination of Cy3-labelled siRNA after injection into the haemocoel indicated the creation of a scenario in vivo that is similar to the soaking technique in vitro (124). In addition, low efficacy in delivery of dsRNA or siRNA might also be attributed to the lack of molecules involved in RNA uptake and transport to allow for systemic spread of interfering RNAs. Recent EST database analyses revealed that H. contortus apparently lacks orthologs for rde-4, responsible for dsRNA recognition and binding, as well as sid-1, sid-2, rde-2 and rsd-2 orthologs, required for dsRNA uptake and systemic spread, whilst dicer and drh-1 involved in dsRNA processing are present (122).

It is difficult to establish reliable numbers Selleck Sirolimus on the disease burden of PID, as there are very different approaches to accessing the incidence and prevalence of PID, including telephone surveys [2] and geographically limited cohort studies [3]. However, patient registries

represent the most common approach, and literature provides a large range of results from these registries that have been organized mainly at the national level [4–6]. Patient registries can work as a powerful tool that fulfils a range of purposes, such as describing the natural history of a disease, determining clinical and/or cost-effectiveness of treatment, assessing safety or harm and measuring or improving quality of care [7,8]. Since 2004, the European Society for Immunodeficiencies (ESID; http://www.esid.org) is running a pan-European registry for primary Wnt inhibitor immunodeficiencies (the ESID database).

The aim of this database is long-term compilation of PID patient data to answer challenging epidemiological questions as outlined above. In addition, the ESID database serves as a basis for outcome-related research questions and to generate research hypotheses that can be tested further in dedicated (clinical) studies. Using the database, researchers have the possibility of identifying patient cohorts for genetic screening and multi-centre trials. Data sets can be extended flexibly for studies on subgroups of patients using the database as a platform for their reporting forms [9,10]. Current

studies include a study on hypogammaglobulinaemia in children (PedPAD; by Esther de Vries, ‘s-Hertogenbosch), a survey on dedicator of cytokinesis 8 (DOCK8)-deficient patients (Michael Albert, Munich) and a survey on chest computed tomography (CT) findings in antibody-deficient patients (Ulrich Baumann, Hanover; http://www.chest-ct-group.eu). Some of the diseases present in the ESID database are also the subject of other rare disease registries. These include registries for autoinflammatory syndromes [11,12]), severe neutropenia [13] and a registry for stem cell transplants in PID [14]. The ESID database co-operates with these registries to ensure a high level of completeness and data quality. ESID provide updates regularly on the development of the database project; this is the third update in this Interleukin-2 receptor series. First analyses on the data collected from 2006 and 2008 have been published previously in this journal [15,16]. The ESID online database is a secure, internet-based patient registry which combines both clinical and laboratory data of PID patients. Patients are grouped into nine main categories. These are predominantly T cell deficiencies, antibody disorders, phagocytic disorders, complement deficiencies, other well-defined PIDs, autoimmune and immunedysregulation syndromes, autoinflammatory syndromes, defects in innate immunity and unclassified immunodeficiencies.