Flow cytometry showed that all three strains were internalized by THP-1 cells but in contrast to the M-cell translocation results, L. salivarius was internalized by THP-1 cells at a higher rate (54%) than E. coli (31%) or B. fragilis (22%; Fig. 6a). Confocal laser scanning microscopic analysis confirmed this observation, (Fig. 6b). In addition, THP-1 cells that were co-incubated with L. salivarius had significantly less production of the pro-inflammatory cytokines IL-1β, IL-6 and TNF-α (P < 0·01 and P < 0·001)

than Dabrafenib THP-1 cells incubated with B. fragilis or E. coli (Fig. 6c–e). In contrast, THP-1 cells co-incubated with L. salivarius had increased production of the chemokine IL-8 compared with THP-1 cells that were co-incubated with B. fragilis or E. coli (P < 0·05; Fig. 6f). The aim of this study was twofold: (i) to assess the translocation of different commensal bacteria across M cells and (ii) to assess the capacity of M cells for immunosensory discriminatory responses to these same bacteria. Although many studies have examined the rate of translocation of pathogens, fewer studies have examined translocation of non-pathogenic commensal bacteria, which are constantly Torin 1 sampled

by M cells within the gut and may even reside in Peyer’s patches under normal physiological conditions.10,20–22 As the normal gut flora belong predominantly to two phyla; the Firmicutes and the Bacteroidetes, we chose L. salivarius and B. fragilis to represent Carbohydrate each of these phyla and a non-pathogenic E. coli as a second common commensal bacterium.23 This study demonstrates that these three different commensal bacteria translocate in vitro across an M-cell monolayer with varying efficiencies. An unexpected finding was that B. fragilis translocated with the greatest efficiency, as previous in vivo studies have shown that it is the least efficient commensal at translocating across

M cells to the mesenteric lymph nodes.24 This discrepancy may be accounted for in part by species differences in M-cell surface properties and function between human cells in culture and gnotobiotic mice as used in the original study. Some M-cell receptor/microbe ligand interactions have been characterized, including β1 integrin/Yersinia spp., α(2,3) sialic acid/reovirus and GP2/FimH-positive bacteria, but it is likely that many more remain to be discovered.25–28 For example, Chassaing et al.29 recently observed that the presence of long polar fimbriae enhances adherent-invasive E. coli translocation in M-cell monolayers, although the respective receptor in this instance was not identified. Microarray analysis of the C2-M cells revealed that each commensal bacterium induced different gene expression patterns in M cells, with E. coli and B. fragilis inducing the most similar gene expression changes.

This inhibitory effect was confirmed in S2 cells stably expressing viral Pellino following lentiviral transduction. Viral Pellino also displayed cytoplasmic localisation upon stable expression (Fig. 2C) and inhibited C106-induced activation of the drosomycin promoter (Fig. 2D). This confirms that the entomopoxviral protein can obstruct a key insect immune–response pathway. The high degree of sequence and mechanistic conservation between insect Toll and mammalian TLR signalling pathways led us to further explore the potential immunomodulatory capabilities of viral Pellino in human cells. Expression of increasing amounts of viral Pellino in HEK293-TLR4 cells (Fig. 3A) showed dose-dependent

inhibition of LPS-induction of an NF-κB-responsive promoter–reporter construct (Fig. 3B). We next confirmed that viral Pellino could block the endogenous NF-κB pathway in a cell selleckchem that was naturally responsive to LPS by demonstrating that lentivirally delivered viral Pellino

blocked the LPS-induced phosphorylation of the NF-κB subunit p65 upon stable expression in U373 cells (Fig. 3C). The regulatory effects of viral Pellino on the NF-κB pathway Navitoclax manufacturer have functional consequences for pro-inflammatory gene expression since the transduction of THP-1 monocytic cells with varying titres of lentivirus, conferring stable viral Pellino expression, caused an inhibition of www.selleck.co.jp/products/ch5424802.html LPS induced expression of the NF-κB-responsive gene IL-8 (Fig. 3D). The highest titre also inhibited LPS induction of TNF

in THP-1 cells (Fig. 3E). These studies confirm the regulatory effects of viral Pellino on TLR4 signalling in a number of cell types. We next investigated the mechanistic basis to the regulatory effects of viral Pellino on TLR signalling. IRAK-1 was an obvious target for viral Pellino, given that the mammalian Pellinos have been shown to associate with IRAK-1 10, 25, probably via their FHA domain, and that the homology modelling studies detailed above suggest the presence of a core FHA domain in viral Pellino. Co-immunprecipitation studies demonstrated that vPellino and IRAK-1 associated upon co-expression. This was observed upon immunoprecipitation of viral Pellino and immunoblotting for IRAK-1 (Fig. 4A). Furthermore, viral Pellino was found to interact with endogenous IRAK-1 upon immunoprecipitation of the latter (Fig. 4B). The IRAK-1-viral Pellino interaction is also apparent under conditions where viral Pellino is expressed at more physiologically relevant levels as facilitated by lentiviral-mediated delivery of viral Pellino into U373 cells (Fig. 4C). Further evidence in support of the IRAK-1-Pellino interaction is provided by co-localisation of IRAK-RFP and viral Pellino-GFP in HEK293 cells (Fig. 4D). Conflicting reports exist on the importance of IRAK-1 kinase activity in the interaction between mammalian Pellinos and IRAK-1 14, 15.

In addition, patients with fibrosis had lower FCRN mRNA levels compared to patients without fibrosis (P = 0·041). No relationship between FCRN mRNA levels and other phenotypical features of CVID (presence of chronic diarrhoea, splenomegaly, granulomas, lymphadenopathy or autoimmune phenomena) LDK378 in vitro was documented. No correlation was found between FCRN mRNA level and pre-infusion IgG and also serum albumin levels

in CVID patients. However, a correlation was demonstrated between FCRN mRNA level and the decline in serum IgG concentration during the second week after IVIg infusion (D14/D7 ratio) (P = 0·045 Spearman’s correlation coefficient). The higher the FCRN mRNA expression, the less pronounced the decrease in IgG concentration in the tracked period after IVIg infusion was observed [6].

We also showed a significant positive correlation between FCRN mRNA expression and the ‘efficiency index’ defined as: [IgG trough level – IgG residual level (g/l)]/IgG dose (g/kg/week [7]; P = 0·05). Selumetinib in vivo We did not document any correlation between FCRN mRNA expression and serum albumin levels in our CVID patients (P = 0·258). Our findings show that FcRn may play a role in the development of lung structural abnormalities, which are the principal life-threatening complications in patients with CVID, as well as in the catabolism of therapeutically administered IVIg. However, our results were obtained in a limited number of patients and show borderline statistical significance, and

need to be interpreted carefully. This study was supported by grant NT 111414-5/2010 of the Czech Ministry of Health. J. L. has received consultation fees from Baxter and LFB Biotechnologies; research selleck inhibitor support from Shire and Baxter; honoraria for lectures from Biotest and Baxter; and support for clinical studies from Octapharma and CSL Behring. “
“Our and others’ previous studies have shown that Schistosoma japonicum (SJ) infection can inhibit allergic reactions. We recently reported that DCs played an important role in SJ infection-mediated inhibition of allergy, which was associated with enhanced IL-10 and T regulatory cell responses. Here, we further compared the role of CD8α+ DC and CD8α− DC subsets for the inhibitory effect. We sorted CD8α+ DC (SJCD8α+ DC) and CD8α− DC (SJCD8α− DC) from SJ-infected mice and tested their ability to modulate allergic responses in vivo. The data showed that the adoptive transfer of SJCD8α− DC was much more efficient than SJCD8α+ DC for the suppression of allergic airway eosinophilia, mucus overproduction, antigen-specific IgE responses, and Th2 cytokines (IL-4 and IL-5).

[36] In a culture-proven case of melioidosis, it is important to rule out soft-tissue https://www.selleckchem.com/products/jq1.html and visceral abscesses by computed tomography of abdomen and pelvis, irrespective of clinical presentation. Abdominal ultrasound is often recommended for children in order to minimize radiation exposure. All cases of melioidosis, irrespective of clinical severity, should be treated with at least 10–14 days (up to 8 weeks in patients with severe disease such as those with ongoing septic shock, deep-seated or organ abscesses, extensive lung disease, septic arthritis, osteomyelitis, or neurologic melioidosis) of initial intravenous intensive therapy, followed by eradication therapy with high-dose

trimethoprim–sulfamethoxazole (TMP + SMX) for a minimum of 3 months (Table 1).[2,

5, 28] Ceftazidime has been in use as the preferred intravenous agent subsequent to the open-label randomized trial from Thailand published in 1989 that demonstrated a significant 50% reduction in mortality rate of severe melioidosis with ceftazidime (120 mg/kg per day) compared with ‘conventional therapy’ (combination of chloramphenicol 100 mg/kg per day, doxycycline 4 mg/kg per day, TMP + SMX 10 + 50 mg/kg per day).[37] With the theoretical advantage of lower minimal inhibitory concentration and more favourable time-kill profile,[38] imipenem has alternatively been shown to be at least as effective as ceftazidime, with no difference in mortality rates in another open-label GDC-0068 nmr randomized trial from Thailand.[39] Moreover, in a retrospective Phosphatidylethanolamine N-methyltransferase study from Australia,

the use of another carbapenem, meropenem has been shown to be associated with improved outcomes in patients with severe sepsis associated with melioidosis.[40] With the exception of doxycycline, the doses of antimicrobials need to be adjusted in patients with impaired renal function and in those receiving renal replacement therapy (Table 2).[41-45] Burkholderia pseudomallei is inherently resistance to penicillin, ampicillin, first-generation and second-generation cephalosporins, macrolides, quinolones and most aminoglycosides, thereby limiting therapeutic options. Primary resistance to ceftazidime is extremely uncommon but occasional secondary resistance has been reported from endemic locations, usually after prolonged therapy.[46-50] Resistance to carbapenems has not been reported yet. Hence, the use of these antimicrobials could be continued as empirical or first-line therapy for both primary and recurrent melioidosis infection, at least until antimicrobial susceptibility testing of the organism is available. The rate of resistance to TMP + SMX, as assessed with the use of Etest has been reported to be up to 2.5% for Australian isolates but much higher at up to 13% for Thai isolates, although current studies across the endemic region are reassessing this issue.

4 months while 12.8% of patients with unilateral high grade stenosis had a rise in serum creatinine over an average follow-up period of 40.1 months.14 Stenosis to the entire renal mass was found to be associated with higher baseline creatinine and greater likelihood of clinical deterioration. In a cross-sectional study involving a cohort of patients from the Cardiovascular Health Study, Edwards et al. analysed the association between ARVD and excretory renal insufficiency.15 The presence of ARVD showed an association with renal insufficiency (odds GDC-0449 in vitro ratio 2.21; 95% confidence interval: 1.02–4.79; P = 0.043) that was independent of effects of age, race, sex, body weight and diabetic status.

The prospective

multicentre observational study by Pillay et al. in 2002 recruited patients with a >50% RAS from patients undergoing angiography for peripheral vascular disease. A total of 159 renal arteries in 85 patients with such stenoses were followed up by renal ultrasound over a mean period of 30 months. Renal length and BP were stable. A significant increase in serum creatinine was noted in the survivors of unilateral disease without intervention.16 The finding of declining renal function in patients with unilateral check details ARVD suggests that intrinsic parenchymal disease, rather than the disease of the large renal arteries is the major determinant of declining renal function in this population. This hypothesis was supported by an elegant prospective study by Farmer et al. that looked at the relationship between presence of RAS and single kidney glomerular filtration rate (SK-GFR) using radionuclide studies in 79 patients with ARVD. The study noted a similar

impairment of renal function in kidneys with and without ARVD while kidneys with occluded renal however arteries were associated with significant reduction in function compared with the contralateral kidney. It was concluded that unilateral ARVD could not only compromise ipsilateral SK-GFR by ischemic mechanisms but also contralateral SK-GFR by non-ischemic mechanisms.17 The study by Losito et al. reported on 195 patients with ARVD over an average follow up of 54 months.18 Of the total, 54 were maintained on medical management, with 38.8% on an ACE inhibitor as one of the many antihypertensives in the medical treatment arm. During the period of follow up, the mean change in creatinine in the medically treated arm was an increase of 108 µmol/L. When worsening renal function was examined by Losito et al. two factors were found to be significant by multivariate analysis. The first was an abnormal baseline creatinine (>128 µmol/L) with a hazard ratio of 1.42. The second was the use of an ACE inhibitor which was associated with a reduced risk of further impairment of renal function (hazard ratio of 0.29), more pronounced in the medically treated arm.

A potential caveat of the above results is that the CD3lo DP cells from Bcl11bdp−/− mice may not represent a pure population of immature,

unselected, DP cells, and might contain cells derived from more mature populations, possibly owing to the difficulty to resolve the mutant cell populations with the CD8, CD4, and CD3 markers. To address this issue, we analyzed the expression of several genes previously found to be induced in WT DP cells during positive selection, using transcriptome data from a published comparison of gene expression profiles of unselected DP cells (CD69− DP cells from Zap70-deficient mice) to selected, Temozolomide cell line CD69hi cells from WT animals 41 (data accessible at Erlotinib datasheet NCBI GEO database accession GSE2262). Although some selection-induced genes were indeed overexpressed in the CD3lo DP cells from Bcl11bdp−/− mice (Zbtb7b, Id2, Klf2, CD53, IL7r, and Irf7), several others were expressed at similar low levels in WT and mutant cells (Itm2a, Nr4a1, Bcl2a1a, Slfn1, Mapk11, Nr4a3, Tnfrsf9,

Acvrl1, Ccr7, Ephx1, Ms4a4b, St6gal1, Tes, Nab2, and Ccl22), suggesting that the mutant CD3lo DP cells do not exhibit a general induction of the gene expression program associated with thymocyte maturation. We selected five of these genes (Ccr7, Slfn1, Ephx1, Ms4a4b, and Mapk11) for further analysis, as these genes displayed strong differences in gene expression levels between unselected and selected cells in the data from Sun et al.41 (>3 log induction), Chorioepithelioma and were thus likely to be informative with respect to the selection/purity status of the analyzed populations. We sorted CD3loDP, CD3+DP, CD3+CD4+ SP, and CD3+CD8+ SP cells from two WT and two Bcl11bdp−/− mice (see Supporting Information Fig. 6 for

sorting gates and purity of the sorted populations) and analyzed the expression of the selected genes in these populations by RT-qPCR (Fig. 7). In WT samples, all five genes were expressed at low levels in CD3lo DP cells and strongly induced in the CD3+ DP and SP populations, thus validating previous microarray results 41. In agreement with our transcriptome data, all five genes were also expressed at very low levels in mutant CD3lo DP cells. Two genes (Ephx1 and Ms4a4b) were strongly induced in the mutant CD3+DP and SP-like populations. This observation reveals that the phenotypically more mature cells from Bcl11bdp−/− mice have retained the capacity to induce a subset of the genes normally upregulated during positive selection.

Conclusion: Treatment of OAB

with solifenacin is associated with significant improvement in generic HRQoL and disease-specific symptoms at 8 weeks after drug administration. check details Particularly for generic HRQoL as measured by the SF-36, solifenacin treatment effectively improves three SF-36 scores: PF, VT, and MH. “
“Objectives: It has been reported that nitric oxide (NO) mainly contributes to prostate or urethral smooth muscles relaxation, and that nitrergic innervation and neuronal NO synthase (nNOS) levels are decreased in benign prostatic hyperplasia. The purpose of the present study was to evaluate the feasibility to gene therapy for benign prostatic hyperplasia by transferring nNOS gene into the rat prostate with in vivo electroporation (EP) procedure. Methods: Male Sprague–Dawley rats were divided

into four groups (sham, only EP, only nNOS injection, and nNOS gene injection with EP groups). Fifty micrograms of luciferase gene and nNOS expression vectors in 50 µL of K-PBS (potassium-phosphate buffered saline) were injected into the prostate. Immediately after the injection of these vectors, the vector injection points were electroporated by the two-square parallel Akt inhibitor electrodes. Two days after gene transfer, luciferase analysis and an immunohistochemical staining for nNOS were performed, and NO2−/NO3− (NOX) release was measured using high-performance liquid chromatography coupled with the

microdialysis procedure. Results: The optimal electric pulse conditions were 50 V, 1 Hz and 10 msec. In vivo EP with these conditions showed the increase in the luciferase gene expression approximately 300-fold of the control group. In the nNOS gene injection with EP group, the marked nNOS immunoreactivity was observed, and NOX release was significantly higher, as compared to other groups. Conclusion: The results suggest that EP is a feasible technique for in vivo gene transfer into the rat prostate, and that the transferred nNOS gene functionally expresses and contributes to NO production. “
“Bladder hypertrophy and dysfunction are well-known bladder responses to outlet obstruction (i.e. urodynamic overload). Cardiac hypertrophy and heart failure are also caused by hemodynamic overload, and Tyrosine-protein kinase BLK many basic and clinical studies suggest that the local renin-angiotensin system (RAS) has a crucial role in load-induced cardiac pathogenesis. The similarity of the response of the heart and the bladder to overload suggests that angiotensin II (AngII) may have a similar regulatory role in pathological remodeling, such as muscle growth and collagen production of the obstructed bladder. Previous in vitro studies show that angiotensin I is converted to AngII by angiotensin converting enzyme (ACE) or chymase, which exists in the human bladder.

SigmaPlot 2002 for Windows version 8.02 (SPSS, Chicago, IL, USA) and Paint Shop Pro

version 7.04 (Jasc Software) were used for conducting statistical analyses and creating graphs. To find the optimal PCR conditions for the selective detection of viable H. pylori, samples containing a mixture of dead and viable bacteria were used. The dead bacteria were produced artificially by treating viable bacterial samples with 70% EtOH for 20 min to obtain dead bacterial cells. Bacterial death was confirmed by the absence of any H. pylori colonies on bacterial culture media (data not shown), although some H. pylori might have acquired viable, selleck chemical but non culturable, forms. Different concentrations of EMA (0, 1, 5, 10, and 50 μM) and PMA (0, 5, 10, 50, and 100 μM) were added to both viable and dead H. pylori samples, in order to determine the ideal conditions for selective removal of genomic DNA from dead bacteria without loss of DNA from viable bacteria. After treatment of EtOH-killed H.

pylori samples with 10 μM EMA, we found that most of the genomic DNA was still present. In addition, treatment of viable H. pylori samples with EMA at concentrations as low as 1 μM resulted in loss of genomic DNA (Fig. 1a), showing that addition of EMA before PCR may not be useful for discriminating between viable and dead bacteria. PMA concentrations of up to 50 μM did not result in loss of genomic DNA from viable bacteria, although loss of genomic DNA did occur at 100 μM PMA (Fig. 1b). In contrast, treatment of EtOH-killed bacteria with PMA resulted

in significant genomic DNA loss for concentrations of up to 10 μM, and not all genomic DNA was detectable Selleckchem SB431542 at 50 and selleck compound 100 μM concentrations (Fig. 1b). Thus, 50 μM was determined to be the most suitable PMA concentration for treating samples before PCR for selective detection of viable H. pylori. To further investigate genomic DNA loss after EMA and PMA treatments, these agents were added to viable and EtOH-killed H. pylori samples at concentrations of 5 μM and 50 μM, respectively; and the amounts of genomic DNA measured and compared by using a spectrophotometer. PMA affected the genomic DNA of viable H. pylori (reduced by 20.4 ± 3.1%, bar B in Fig. 2), but had a significant effect (P < 0.05) on dead bacteria with removal of most genomic DNA (reduced by 91.1 ± 1.2%, bar E in Fig. 2). In contrast, EMA had also a significant effect (P < 0.05) on the genomic DNA of viable H. pylori causing a DNA loss of about 77.3 ± 3.9% (Fig. 2). Viable and dead H. pylori cells were examined under a fluorescence microscope after addition of SYTO 9 and EMA and SYTO 9 and PMA to test the ability of EMA and PMA to pass through the cell membranes (Fig. 3). SYTO 9 plus PMA treated viable bacteria were not stained since PMA cannot penetrate viable H. pylori (Fig. 3a) but these bacteria exhibited a green color due to SYTO 9 (data not shown). In contrast, dead bacteria were stained because PMA can penetrate them (Fig. 3b).

Our work highlights the differences that can be observed when monitoring the clinical and immunologic function in these patients within the context of different mutations, but even more the clinical and immunologic effects in the revertant phenotype once they are under the effects of the ERT with PEG-ADA. Our findings might provide additional PXD101 price insight into the effects of immune reconstitution

by gene therapy in ADA deficiency, particularly in patients who have been treated previously with ERT. We deeply appreciate the commitment of our patient and his parents to perform these studies. Acknowledgments are made to Carlos J. Montoya, Olga L. Morales, Alejandra Wilches, Dagoberto Cabrera and Yadira Coll for their dedication to the care of our patient. We also thank the Grupo de Inmunología Celular e Inmunogenética (University of Antioquia, Medellín, Colombia) for their help with the HLA typing and Christiam Álvarez for his technical support. This work was supported by a grant from the “Estrategia para Sostenibilidad 2009–2011” 9889E01489 (CODI, UDEA) and the Group of Primary Immunodeficiencies and the Fundación “Diana García de Olarte” para las Inmunodeficiencias Primarias -FIP- (Medellín,

Colombia). “
“The nature of pathogenic mechanisms associated with the development of multiple sclerosis (MS) have long been debated. However, limited research was conducted to define the interplay between infiltrating lymphocytes and resident cells of the central nervous Selleckchem Talazoparib system (CNS). Data presented in this report describe a novel role for astrocyte-mediated alterations to myelin oligodendrocyte glycoprotein (MOG)35–55-specific lymphocyte responses, elicited during the development of experimental autoimmune encephalitomyelitis (EAE). In-vitro studies demonstrated that astrocytes inhibited the proliferation and interferon (IFN)-γ, interleukin (IL)-4, IL-17 and transforming growth factor (TGF)-β secretion levels of MOG35–55-specific lymphocytes,

an effect that could Selleck Neratinib be ameliorated by astrocyte IL-27 neutralization. However, when astrocytes were pretreated with IFN-γ, they could promote the proliferation and secretion levels of MOG35–55-specific lymphocytes, coinciding with apparent expression of major histocompatibility complex (MHC)-II on astrocytes themselves. Quantitative polymerase chain reaction (qPCR) demonstrated that production of IL-27 in the spinal cord was at its highest during the initial phases. Conversely, production of IFN-γ in the spinal cord was highest during the peak phase. Quantitative analysis of MHC-II expression in the spinal cord showed that there was a positive correlation between MHC-II expression and IFN-γ production.

Thus, the

primary cellular target of IL-23 in the context of autoimmunity is a subject of some debate. Innate lymphoid cells (ILCs) are a recently discovered family of lymphocytes being involved in early host defense, particularly at mucosal epithelial surfaces. Given the fact that RORγt-dependent ILCs (group 3 ILCs) constitutively express the IL-23-receptor, and that they have been implicated in intestinal autoimmunity, we hypothesized that ILCs could contribute to the early development of autoimmune neuroinflammation. Through systematic analysis, we detected a sizable population of Thy1+ Sca1+ ILCs in the inflamed CNS tissue. CNS-infiltrating ILCs were characterized by expression of the IL-7-receptor and production of proinflammatory IL-17 and IFN-γ. Furthermore, PLX-4720 supplier genetic fate-mapping revealed their dependence on the transcription factor RORγt. However, upon specific in vivo ablation of this cell population, we found that they do not influence the course of the disease. Over the past 5 years, the term innate lymphoid cells (ILCs) has been coined to describe a new family find more of innate lymphocytes that lack

rearranged antigen receptors, but share phenotypic and functional characteristics with cells of the adaptive immune system. Beside the well-characterized populations of natural killer (NK) cells and lymphoid tissue inducer cells, several subtypes of ILCs Vitamin B12 have recently been described, both in mouse and human (reviewed in [1, 2]). RORγt+ ILCs, which depend on the retinoic

receptor related orphan receptor (RORγt) for their development, constitutively express the IL-23 receptor and are able to produce pro-inflammatory cytokines such as IL-17 and IL-22, similar to T cells of the TH17 lineage [3]. In contrast, the so-called group 2 ILCs (also known as nuocytes or natural helper cells) were discovered as innate producers of IL-5 and IL-13 [4, 5]. Very recently, a group of researchers has proposed a unifying nomenclature for ILCs, which would divide these cells into three subgroups based on their phenotypic and functional profile [6]. RORγt+ ILCs (group 3 ILCs) are best known for their nonredundant role during formation of secondary lymphoid tissues in embryonic development [7], but they also have been suggested to be critical in early host defense in different mouse models of infection, in particular in the intestine. For example, after infection with Citrobacter rodentium, CD4+ Thy1+ ILCs respond by production of IL-22 required for bacterial clearance [8]. Furthermore, Nkp46+ ILCs have been implicated in the maintenance of intestinal homeostasis [9, 10]. In 2010, another unexpected role was attributed to RORγt+ ILCs: Powrie and colleagues identified a Lineage− Thy1+ Sca1+ population of ILCs as the main mediator of innate IL-23-dependent gut inflammation in Rag−/− mice after infection with Helicobacter hepaticus [11].