Our understanding of the basic immunobiological properties of DC has been significantly advanced over the years. This has not only provided good explanations for the problems encountered, but also stimulated many new

ideas regarding the potential ways forward aimed to improve DC therapy in a more fundamental way. The important issues lie within DC heterogeneity and functional plasticity, and hence their immunogenic versus tolerogenic properties or potentials. Selleckchem CH5424802 It has gradually become clear that DC are not a homogeneous population, and questions have also been raised about the origin and nature of the monocyte-derived, DC-like cells generated in vitro 27. The ability of these cells to provide activation signals, of both antigen-specific and non-specific triggers, can vary vastly among DC subsets or lineages, and depends on their functional status 28–31. Among them, a unique human DC subset (CD11c+CD141+), with superior antigen cross-presentation capacity and expressing the XC chemokine

receptor 1 (XCR1+), has recently been identified by several groups as the homologue of mouse CD8α+ DC 32–35. As with their murine counterparts, this type of DC was found to be effective activators of CD8+ cytotoxic T cells, which Acalabrutinib in vivo may have important implications in the design of new human DC vaccines. Moreover, in addition to subset-dependence, the functional properties of DC are also associated with the maturation status of the cell. Immature DC are in a so-called “antigen-uptake mode”, with low cell surface expression of MHC class I and class II molecules, which

can be rapidly enhanced upon exposure to maturation or activation signals, acquiring subsequently the “antigen-presenting mode”. The low MHC expression may therefore affect the ability of immature DC to present antigen to T cells. Under certain conditions, DC can even exert tolerogenic effects by producing immunosuppressive molecules, SPTBN5 or by inducing regulatory T cells, to inhibit the immune system 1, 8, 24, 36. The concept of tolerogenic DC has become far more appreciated. It is now recognised that while immunogenic DC play an important role in host defence, their tolerogenic counterparts are crucial for the maintenance of self-tolerance, being part of a built-in mechanism to avoid autoimmunity 37. It has been demonstrated that, under the tumourigenic microenvironment, the host DC possessed a typical tolerogenic, or regulatory, phenotype 38. DC, as a double-edged sword, can therefore induce either active immunity or tolerance depending on their functional conditions. The types and functional status of DC, hence the immunogenic “quality” or nature of the cell vectors employed for tumour vaccine delivery, are therefore of critical importance. Various attempts have subsequently been made in order to generate DC with a highly immunogenic phenotype.

Sustained suppression of the B cell compartment can lead to impairment of T cell responses, resulting in a prolonged immunosuppressive

state with an increased risk of vertical transmission of cytomegalovirus (CMV) infection from mother to fetus [112]. Pan-specific depletion of B cells can deplete autoantibodies as well as protective natural antibodies and regulatory B cell subsets [5]. Therefore, it is clear that carefully planned clinical trials are needed to evaluate HM781-36B mw the full benefits and harms of rituximab in pregnancy before it can be recommended for wider use in pregnancy. The evidence presented in this review has clearly highlighted the important role of B cells in shaping pregnancy outcomes that have implications for long-term Carfilzomib supplier human health. Despite this, there are still limited data detailing the changes in the human B cell compartment, and the role of B cell subsets in pregnancy outcomes is poorly studied. This is due to the limited

number of B cell markers used in earlier studies to describe changes in B cell subsets during pregnancy. Recent advances in B cell biology indicate clearly that these markers alone are not adequate in describing their full functions in human pregnancy. Further efforts should be dedicated to delineate the contribution of these B cell subsets in the maintenance of a healthy pregnancy as well as their roles in pregnancy complications. In light of the potential benefits of rituximab in depleting autoreactive B cells and the emerging safety profile of rituximab in pregnancy, it is anticipated that B cell depletion therapies will eventually be trialled in obstetric complications that involve autoantibodies such as APS, SLE or ITP. It is reasonable to expect that rituximab will make some advances in the treatment of refractory conditions in pregnancy and provide a viable option that spares the use of high doses of chemotherapeutics

and steroids in high-risk pregnancy to reduce risk of fetal toxicity [115], and thereby allows the pregnancy a better chance to develop to full term. Future pilot studies into the Demeclocycline safety and efficacy of rituximab in pregnant patient cohorts are needed to provide a rational basis for larger studies. Although B cell depletion has demonstrated clinical benefits for maternal conditions in high-risk pregnancies, its potential benefits and risks for neonatal outcomes have not yet been investigated fully. It remains to be determined whether or not B cell depletion can improve neonatal outcomes on preterm birth, low birth weights, congenital malformations and their associated long-term health consequences.

The observation that the BTN3 (CD277)-specific mAb 20.1 activates Vγ9Vδ2 T cells and that the BTN3-specific mAb 103.1 inhibits PAg-induced activation provided the first evidence for a role of BTN3 in TCR-mediated activation of Vγ9Vδ2 T cells [8, 9]. Furthermore, mAb 20.1 induces changes in the cell-surface distribution of BTN3 similar to those seen after treating Selleckchem Regorafenib human BTN3A1-expressing cells with aminobisphosphonates [8, 9]. BTN3A1 differs

from the other members of the BTN3 family (BTN3A2 and BTN3A3) mainly by its intracellular domain [8-10], which most recently has been shown to contain a PAg-binding site [10], and in aminobisphophonate-induced membrane distribution. These observations [8, 9] and the fact that PAg binding to the extracellular domain of BTN3A1 has not been demonstrated [8-11] have led to models of PAg- and mAb 20.1-induced Vγ9Vδ2 T-cell activation in which PAg and mAb 20.1 induce changes in surface distribution of BTN3A1. These changes may then result in ligation of Vγ9Vδ2 TCR and subsequent cellular activation, either directly or indirectly by recruitment of unknown Vγ9Vδ2 TCR-ligands. Vavassori and colleagues [12] reported experiments with mouse-human hybrid cell lines as presenters of PAg and cells from Vγ9Vδ2 TCR-transgenic

VX 809 mice as the reporter of TCR-mediated OSBPL9 activation, which mapped

control of PAg-presentation to a BTN3A1-containing region of human chromosome 6 (Chr6). The same study confirmed the requirement of BTN3A1 for PAg-mediated Vγ9Vδ2 T cell stimulation by means of knock down and over-expression of BTN3A1 in human cell lines [12]. The authors provided also a wealth of biochemical evidence for binding of PAg to the extracellular domain of BTN3A1 and binding of BTN3A1-PAg complexes to the Vγ9Vδ2 TCR [12]. These results could be interpreted to indicate that chromosomal localization of BTN3A1 fully explains the capacity of Chr6-bearing rodent cells to present PAg. We show now that BTN3A1 expression alone is not sufficient for PAg presentation, since rodent cells transduced with BTN3A1 do allow Vγ9Vδ2 TCR-mediated activation by mAb 20.1, while rodent cells carrying Chr6 can present PAg to Vγ9Vδ2 T cells. An important obstacle when studying the role of BTN3 in PAg-induced Vγ9Vδ2 T cell activation is that most human cell types, including Vγ9Vδ2 T cells, present PAg and express BTN3. To avoid PAg presentation by Vγ9Vδ2 TCR-positive cells, Vγ9Vδ2 TCR-transduced murine cells can be used as reporter cells, since rodents, like most nonprimate mammals, lack BTN3 [13] and do not present PAg (reviewed in [7] and J. L., M. M. K., L. S., T. H. unpublished data).

A summary of the four landmark anaemia trials

is described in Table 1. The Normal Haematocrit Cardiac Trial compared the effect of normal haematocrit (42 ± 3%) to lower haematocrit (30 ± 3%) in 1233 haemodialysis patients with cardiac disease on the composite outcome of death and non-fatal myocardial infarction.9 The dose of erythropoietin was increased by 50% at randomization in the normal haematocrit group. The trial was stopped early on the third interim analysis by the safety and data monitoring committee because more patients in the normal haematocrit group achieved the primary end-point (risk ratio (RR) 1.3, 95% confidence interval (CI) 0.9–1.9). The difference in the primary end-point between the groups, though not statistically significant, was sufficient to make it very unlikely that continuation of the study would reveal a benefit for the normal haematocrit group. Erlotinib chemical structure Results were also nearing the statistical boundary of a higher mortality rate in the normal haematocrit group. Mean erythropoietin doses at the end of the study in the normal and lower haematocrit groups were 440 U/kg per week and 120 U/kg per week, respectively. The event rates of death or myocardial infarction among the normal haematocrit group remained higher than the lower haematocrit group Ceritinib manufacturer at every level of achieved haematocrit. This finding suggests that requirement

of high-dose ESA to achieve a certain haemoglobin level rather than high haemoglobin may have been the cause of poor outcomes. Teicoplanin In the lower haematocrit group, mortality rates were lower in patients who achieved higher haematocrit. In the normal haematocrit group, event rates were lowest in patients who achieved a haematocrit level of 39–41.9%. When both groups were combined, each 10 points rise in haematocrit was associated with a 30% reduction in mortality (RR 0.7, 95% CI 0.6–0.8). These results raise the possibility that failure to achieve high haemoglobin concentrations rather than high haemoglobin concentrations per se may have been responsible for the poor outcomes. Kilpatrick

et al. reported a post-hoc analysis of 321 participants from the normal haematocrit group.11 In these patients, the dose of erythropoietin was increased by 30–70% at randomization and erythropoietin responsiveness was measured over the next 3 weeks as a ratio of weekly haematocrit change per 1000 IU/week increase in the dose of erythropoietin. Mortality rates decreased from 34% in the lowest quartile of erythropoietin response to 14% in the highest quartile. In the adjusted Cox proportional hazard model, the adjusted hazard ratio (HR) for mortality for the highest quartile was 0.41, (95% CI 0.20–0.87) compared with the lowest quartile of erythropoietin response. Participants in the highest quartile group were receiving a lower dose of erythropoietin than the combined group of the three remaining quartiles (mean 17 893 IU/week vs 29 865 IU/week), even though the mean haematocrit levels were similar (42.

The same type of postulates can be applied to pattern recognition receptors in general. This article is protected by copyright. All rights reserved AZD1208 research buy “
“Immunoglobulin (Ig) G replacement therapy is well tolerated by the majority of recipients; however, isolated or recurrent adverse events occur in about a third of patients. Thrombosis has been a recognized complication of IgG infusion for the past 20 years [1]. All forms of thrombotic disease have been recognized including, but not limited to, thrombotic

microangiopathy, deep vein thrombosis, myocardial infarction, stroke, pulmonary embolism and transfusion-related acute lung injury (TRALI). These are thought to occur more often with intravenous (i.v.) infusion, but are also associated more rarely with subcutaneous (s.c.) therapy. In 2010, the Center for Biologics Evaluation and Research (CBER) at the Food and Drug Administration (FDA) identified individuals in a health-care database who had

received IgG therapy (n = 11 785) and had a thrombotic event on the same day, with the aim of ascertaining the frequency of these thrombotic events and the differences in frequency, if any, between IgG products [2]. Between January 2008 and September 2010, approximately 1% of the study population (n = 122) experienced thromboembolic adverse events (TAEs); the per-infusion rate, although not investigated, would be lower because patients received multiple infusions during the study time-frame. Variances in rates of TAEs between different IgG products were also noted, with an approximately Daporinad price three-fold variation overall. The extension of the retrospective study (2008–11) looked at hyperimmune globulin products; the overall rate of TAEs was reported at one-tenth of that

in the initial study (< 0·01%); however, the highest rates were very similar to those observed previously [3]. The predominant mechanism responsible for these TAEs is thought to involve activated factor XIa. In 2010, an investigation following a cluster of TAEs associated with a single IgG product [4] identified activated factor XIa as a probable procoagulant contaminant. Significant levels of factor XIa have been found in all cases where gammaglobulin Loperamide preparations associated with thrombosis have been studied; other possible procoagulant contaminants have also been found, but their roles are yet to be defined. Differential content of factor XIa between IgG products correlates with the observance of TAEs, and those products associated with the highest rates of TAEs have the highest level of factor XIa activity. However, this activity alone does not completely predict TAEs; these have been seen to occur with products containing relatively low factor XIa levels and vice versa.

S2) had no effect on BMP induction of hepcidin mRNA. To test whether the suppressive effect of growth factors could be relevant in vivo, we PD0325901 mouse injected mice with EGF, holotransferrin, or their combination (Fig. 3), using recombinant human EGF because of much lower cost. Increased expression

of the known EGF target transcript osteopontin confirmed that EGF had a detectable effect in the liver (Fig. 3B). EGF significantly suppressed hepcidin responses to holotransferrin (Fig. 3A), with hepcidin mRNA approximately 20-fold lower than in mice that received holotransferrin alone. In primary mouse hepatocytes transfected with hepcidin promoter-luciferase reporter, HGF strongly suppressed the induction of the hepcidin promoter by BMP2 (Fig. 4A). We tested a broader range of BMPs in HepG2 cells transfected with hepcidin-luciferase reporter and found that HGF suppressed the induction of the hepcidin reporter by BMP-2, 4, 6, and 9) (Fig. 4C; Supporting Fig. S3A). Thus, HGF is a broadly active transcriptional

suppressor of the BMP response of the hepcidin promoter. We also tested the effect of HGF on another BMP-sensitive luciferase reporter containing the BMP-responsive element CX-4945 in vivo (BRE) from the promoter of the gene for ID1 (inhibitor of DNA binding 1), a known direct target gene for BMP.16 In transfected mouse hepatocytes and HepG2s, HGF suppressed the induction of the BRE-luciferase reporter by BMP-2, -4, -6, and -9 (Fig. 4B,D; Supporting Fig. S3B). Further, in primary mouse hepatocytes HGF and EGF similarly modulated the BMP-dependent induction of ID1 mRNA (Supporting Fig. S4). Taken together, these data indicate that HGF and EGF inhibit transcription of BMP-sensitive

genes including hepcidin, likely by modulating BMP pathway signaling or BMP-dependent assembly of transcriptional machinery. When BMPs bind to their receptor (BMP-R), the receptor phosphorylates and activates cytosolic signaling proteins R-Smads 1, 5, and/or 8, which form complexes with the common mediator Smad4. These complexes translocate into the nucleus where they Oxymatrine transactivate BMP-dependent transcription.19 The induction of hepcidin mRNA by BMP6 occurred within 4 hours, and costimulation with HGF or EGF suppressed the maximal induction of hepcidin mRNA within the same timeframe (Supporting Fig. S5). The short timeframe favored a mechanism based on rapid, covalent modifications of signaling mediators rather than the synthesis of new transcriptional regulators. We hypothesized that HGF and EGF were initiating kinase signaling that resulted in decreased activation of Smad1/5/8, or in inhibitory modification of Smad1/5/8, through prevention or removal of the activating C-terminal phosphorylation20 or by targeting Smads 1/5/8 for degradation. BMP-dependent activating phosphorylation of Smad 1/5/8 was equal in the growth factor-treated and BMP-only series (Fig.

1) and reported by more than 10% of cases. Dental procedures, blood transfusions, and healthcare encounters that do not identify a specific healthcare procedure (e.g., overnight hospital stay or emergency room visit) were not included in multivariate models. A second multivariate model was constructed using interview data that were changed after medical chart review. A third model containing only acute hepatitis B cases and their matched controls was also constructed. Data were analyzed using SAS version 9.1 (SAS Institute Inc., Cary, NC). Population-attributable risks were calculated for exposures that were independently associated

with acute hepatitis B or C infection in the multivariate models.17 A total of 71 cases of acute hepatitis B and acute hepatitis Ceritinib manufacturer C among noninstitutionalized individuals 55 years or older were identified from 2006 to 2008 by the three participating health departments. Two additional cases were deemed

ineligible because they occurred in institutionalized persons: one in a correctional facility and the other in a long-term care facility. Fifty-eight (82%) of the seventy-one eligible cases were acute hepatitis B, and 13 (18%) were acute hepatitis C. Fifty-nine (83%) cases were identified in New York and 12 (17%) in Oregon (Table 1). Of the 71 cases identified, 48 (68%) were enrolled in the study. Of the 23 cases not enrolled, 13 (57%) declined to participate in the study, 7 (30%) were lost to follow-up (i.e., after being interviewed to complete the standard surveillance case report form), IWR-1 purchase and 3 (13%) were unable to consent (e.g., because of a language barrier). Enrolled and

nonenrolled cases were not significantly different with regard to age category, study site, sex, race or ethnicity, and acute hepatitis diagnosis (Table 1). It was not possible to calculate the overall participation rate among controls because telephone Oxaprozin screening of potential controls was terminated in many instances before it could be determined whether any household members met the age requirements for case matching. However, participation was 60% among potential controls who were successfully contacted and indicated that they met the age criteria. All of the 48 enrolled case patients reported symptoms of acute hepatitis with discrete onset of symptoms, consistent with requirements of the surveillance case definitions. From onset of symptoms to study enrollment and interview, the median interval was 10 weeks. Jaundice was reported by 67% of case patients. Symptoms of acute hepatitis were listed as a primary indication for viral hepatitis diagnostic testing by 79% of the case patients. Insurance status among cases and controls was similar, with 2% of cases and 3% of controls reporting that they were uninsured; similar percentages of cases (56%) and controls (55%) reported Medicaid or Medicare coverage.

The effect of H. pylori on host immune function may protect against CD. Alternatively H. pylori may be a surrogate marker for childhood exposure to other gastrointestinal infections and an altered microbiome that is protective. G CHEN, P SAXENA, G COLLINS, RW LEONG Gastroenterology and Liver Services, Concord Hospital, Sydney Local Health District, Sydney, NSW, Australia Background: Infliximab has an established role in management of patients with inflammatory bowel diseases (IBD). The recent Product Information change of 1-hr infusions may improve efficiency, reduce nursing time and cost and improve patient satisfaction but is not widely adopted presently. This

study aims to determine the safety, cost effectiveness and patient satisfaction in patients undergoing traditional 2-hr and accelerated 1-hr infliximab infusions. Methods: This was a retrospective analysis of 1-hr infliximab infusion data. All patients are routinely asked to submit a 10-point Likert scale Enzalutamide in vitro satisfaction questionnaire. Infusion times, adverse events and questionnaire scores were abstracted. Direct nursing cost was calculated per infusion. The primary outcome was adverse events and the secondary outcomes were cost, time saving per infusion associated with an accelerated infusion protocol and patient satisfaction scores. Results: A total of 251 and 75 infusions were administered in the 2-hr (n = 56 patients) and

1-hr group (n = 21 Selleckchem CH5424802 patients) respectively (mean infusion times 136 min vs 60 min, P < 0.0001). The adverse reaction rate of the standard protocol was 3.6% (95% CI: 1.8–6.8%) and accelerated protocol was 0% (95% CI: 0–5.8%; P = 0.125). There was a 44.1% relative

reduction of direct cost of nursing per infusion in the accelerated protocol group. The mean patient satisfaction score was 9.1/10 (95% CI: 8.4–9.9) in the accelerated protocol group compared to 8.5/10 (95% CI: 7.9–9.1) in the standard protocol group (P = 0.19). Conclusions: Accelerated 1-hr infliximab infusions are not associated with an increase in adverse events in treating IBD. There is significant reduction in nursing time and therefore cost when accelerated infusions are utilized. Furthermore, patients report high levels of satisfaction. Therefore, increased Calpain patient freedom and improved efficiency in healthcare delivery can be expected. JA HOLMES,1–3 NA SKINNER,3 M CONGIU,2 R MILLEN,3 SJ BELL,1 T NGUYEN,1 DM ISER,1 DS BOWDEN,4 W SIEVERT,5 PV DESMOND,1,2 K VISVANATHAN,2,3 AJ THOMPSON1–3,6 1Gastroenterology, St Vincent’s Hospital Melbourne, 2Department of Medicine, University of Melbourne, 3Immunology Research Centre, St Vincent’s Hospital Melbourne, 4Victorian Infectious Diseases Reference Laboratory, Melbourne, 5Gastroenterology, Monash Health, Melbourne, 6Gastroenterology, Duke Clinical Research Institute, Durham, USA Background: IL28B genotype (gt) is strongly associated with SVR in HCV-1 patients treated with interferon-based therapy, but the underlying mechanism remains poorly understood.

In vitro experiments using gastric tumor cell lines, murine models and one clinical study provided evidence for a potential role of PAR2 in Helicobacter pylori-induced gastritis. Aim:  To investigate PAR2 expression in H. pylori-infected patients and correlation with proinflammatory IL-8, IL-1β as well as histologic changes of the mucosa. Furthermore, PAR2 expression was studied in context to mucosal see more amounts of secretory leukocyte protease inhibitor (SLPI), a putative

regulator of PAR2. Methods:  Twenty-two H. pylori-infected patients and 72 H. pylori-negative subjects underwent upper GI endoscopy. In antrum-derived mucosal biopsies, PAR2, IL-1β, Alectinib IL-8, and SLPI expression was analyzed by quantitative RT-PCR, and in part by ELISA and immunohistochemistry. Histopathologic evaluation of gastritis was performed according to the updated Sydney classification. Results: IL-8 gene expression was 5-fold increased in the mucosa of H. pylori-infected patients compared with

non-infected (p < .0001), whereas no differences for PAR2 and IL-1β mRNA amounts were observed between both groups. PAR2 gene expression correlated positively with transcript levels of IL-8, IL-1β as well mucosal SLPI levels in H. pylori-infected patients (r: 0.47–0.84; p < .0001), whereas no correlation was found with the degree of gastritis. Conclusions:  PAR2 represents an additive pathway of IL-8 secretion and proinflammatory effects in H. pylori-induced gastritis. Reduced SLPI

levels leading to higher serine protease activities in the mucosa of infected subjects might regulate PAR2 activation. “
“Background:  High-molecular-weight cell-associated proteins (HM-CAP) assay is the most popular serological immunoassay worldwide and has been developed from US isolates as the antigens. The accuracy is reduced when the sera are from adults and children in East Asia including N-acetylglucosamine-1-phosphate transferase Japan. To overcome the reduced accuracy, an enzyme immunoassay using Japanese strain–derived HM-CAP (JHM-CAP) was developed, in which the antigens were prepared by exactly the same procedure as HM-CAP. The performance of JHM-CAP was better than that of HM-CAP in Japanese adults as well as in children. The higher sensitivity was because of the presence of 100-kDa protein that was absent in the preparation of HM-CAP antigen. Materials and Methods:  Immunoblot analysis and peptide mass fingerprinting methods were used to identify the distinctive 100-kDa protein present in JHM-CAP antigens. The peptide sequence and identification were analyzed by Mascot Search on the database of Helicobacter pylori. The identified protein was confirmed by immunoblot with a specific antibody and inhibition assay by the sera.

(2010). The lineage resolved as sister to Scenedesmaceae, Neochloridaceae, and Hydrodictyaceae comprises two desert soil crust isolates, for which we propose a new genus name, Rotundella. Only UTEX B2979 remains alive to date, and for this strain, we propose a new species name R. rotunda. We also erect a new monotypic family, Rotundellaceae, to accommodate this lineage that currently only comprises coccoid soil inhabitants with rarely occurring asexual flagellated stages. Pseudomuriella also does not appear associated with any recognized family in Sphaeropleales. The genus currently comprises four cryptic species, and the

genetic diversity within this genus was described in Fučíková et al. (2011b). We erect the family Pseudomuriellaceae to harbor this lineage. Pseudomuriella is a multinucleate, selleck inhibitor polyplastidic alga that lacks pyrenoids and may easily be confused with Bracteacoccus. While zoospores have been reported in Pseudomuriella (Kalina and Punčochářová 1987), they have not been examined in detail using EM. The fusiform aquatic genus Schroederia, represented in this study by the type species S. setigera (Schröder) Lemmermann, is currently classified as a member this website of Characiaceae. However, this family is now known to be polyphyletic, containing members of Sphaeropleaceae (Ankyra)

as well as Neochloridaceae (Characiopodium), and volvocalean algae such as Characium and Chlamydopodium (reviewed in Lewis and McCourt 2004). Our results suggest that Schroederia should be placed in a separate family, for which we propose the name Schroederiaceae. This family likely also includes the genus Pseudoschroederia (relationship with Schroederia shown in Shoup and Lewis mafosfamide 2003). The ultrastructure and reproduction of Schroederia and Pseudoschroederia were examined by Hegewald and Schnepf (1986), who described the algae as uninucleate, monoplastidic, and reproducing asexually via autospores or biflagellate zoospores. Pyrenoids in this family are enclosed in starch sheaths and are not invaginated

by thylakoids. A morphology-based revision of the Radiococcaceae was published by Kostikov et al. (2002), and included a number of genera. Of these, our study only included representatives of Radiococcus and Planktosphaeria. Figure 2 shows that the sister group to Radiococcus is the genus Follicularia, which we herein include in Radiococcaceae. Kostikov et al. (2002) also included Schizochlamydella in this family, but it was since shown to be closely related to the trebouxiophyte Oocystis (Wolf et al. 2003). Planktosphaeria grouped strongly with Schizochlamys, but because a considerable phylogenetic distance separates Radiococcaceae and these two genera and because their sister relationship was only weakly supported, we propose a new family name, Schizochlamydaceae, for the clade containing Planktosphaeria and Schizochlamys.