As shown in Fig. 1A, significantly more dead Hydroxychloroquine in vivo and apoptotic cells, as judged by staining with 7-amino-actinomycin D (7-AAD) and annexin V, respectively, were presented in anti-CD3+IL-2-activated WT CD8+ T cells (54 and 72%, respectively) than in similarly activated TNFR2−/− CD8+ T cells (13 and 17%, respectively). In contrast, essentially identical 7-AAD and annexin V staining data were obtained for both WT and TNFR2−/− CD8+ T cells when monoclonal anti-CD28 antibodies were included in the AICD assays (data not shown). These results indicate that AICD in either WT or TNFR2−/− CD8+ T cells is not regulated by CD28 costimulation. We have reported previously that TNFR2−/− CD8+ T cells

undergo suboptimal proliferation relative to WT CD8+ T cells when stimulated by anti-CD3 antibodies 6. This observation is consistent with the hypothesis that TNFR2 participates in the optimal activation of anti-CD3-stimulated CD8+ T cells. Here, we found that anti-TNFR2 antibodies also inhibited the proliferation of anti-CD3 stimulated WT CD8+ T cells (Fig. 1B). The specificity of the blocking anti-TNFR2 antibody was demonstrated by its lack of effect on the proliferation of anti-CD3-activated TNFR2−/− CD8+ T cells. This result indicates that in WT CD8+ T cells, optimal proliferation after anti-CD3

stimulation is dependent on TNFR2. We next determined whether antibody-mediated blocking of TNFR2 in WT CD8+ T cells recapitulates the effect of the TNFR2−/− mutation in AICD. We found that the blocking NVP-BKM120 order anti-TNFR2 antibody dramatically increased the resistance of activated WT CD8+ T cells to AICD (Fig. 1C). The specificity of the blocking anti-TNFR2 antibody was again demonstrated by its lack of effect on AICD of TNFR2−/− CD8+ T cells. These data indicate that TNFR2 is essential in

both the optimal proliferation of anti-CD3-activated CD8+ T cells and for the induction of AICD that terminates the proliferative response. To test the hypothesis that intracellular levels of TRAF2 regulate AICD, we determined MTMR9 the expression level of TRAF2 in TNF-α-stimulated WT and TNFR2−/− CD8+ T cells. WT and TNFR2−/− CD8+ T cells were stimulated for 48 h with anti-CD3+IL-2 followed by stimulation with TNF-α for various times. Immunoblotting showed that the amount of TRAF2 protein in WT cells decreased by 6 h after adding TNF-α (Fig. 2A). In contrast, the amount of TRAF2 protein in TNFR2−/− cells remained unchanged, even after 12 h of TNF-α stimulation. Furthermore, we found that TRAF2 protein levels were lower in WT CD8+ T cells than in TNFR2−/− cells at 72 h after anti-CD3+IL-2 stimulation (Fig. 2B). These data indicate that TNFR2 signaling promotes the degradation of TRAF2 at a time when AICD occurs and suggests that intracellular levels of TRAF2 play a critical role in regulating AICD. We next determined the effect of TNFR2 blocking on intracellular TRAF2 levels.

OCT offered the second best sensitivity but displayed the lowest specificity. CLSM and KOH preparation showed a high specificity and CLSM offered the best positive predictive value, similar to KOH preparation and OCT. Fungal culture showed the lowest sensitivity and the worst negative predictive value, yet culture and PCR are the only techniques able to identify genus and species. In summary, CLSM was comparable to PAS staining and superior to KOH preparation. Due to the low specificity we assess OCT not as appropriate. In the differentiation of species PCR outplays the fungal culture in terms of

time and sensitivity. “
“Candida africana is a recently described opportunistic yeast pathogen that has been linked to vaginal candidiasis. This yeast was first described, in 1995, as atypical chlamydospore-negative Candida Bioactive Compound Library albicans strain,

and subsequently proposed as a new Candida species on the basis of morphological, biochemical and physiological characteristics clearly different from those of typical C. albicans isolates. Phylogenetic studies based on the comparison of ribosomal DNA sequences demonstrated that C. africana and C. albicans isolates are too closely related to draw any conclusions regarding the status of a new species. Therefore, on the basis of these studies, some authors considered C. africana as a biovar of C. albicans even if genetic differences may be found if additional regions of genomic DNA are sequenced. mafosfamide The taxonomic situation of C. LDE225 ic50 africana and its phylogenetic relationship with other Candida species is still controversial and remains, at present, a matter of debate. Our goal is to review the current knowledge about C. africana and highlight the development of rapid and accurate tests for its discrimination from C. albicans, Candida dubliniensis and Candida stellatoidea. Furthermore, through the analysis of literature data, we have found that C. africana has a worldwide distribution and a considerable number of features making its study particularly interesting. “
“Invasive fungal infections cause significant morbidity and mortality

in immunocompromised patients. Azoles, and fluconazole in particular, are very active against Candida albicans, and are used widely because of their good tolerability. However, the increasing use of azole antifungals for the treatment of mucosal and systemic Candida infections has resulted in the selection and/or emergence of resistant Candida strains. The main mechanisms of azole resistance among Candida species are the development of bypass pathways, alterations in the ERG 11 gene encoding the azole target enzyme, and the up-regulation of genes encoding efflux pumps. A better understanding of the mechanisms and clinical impact of antifungal resistance is essential to prompt and efficient treatment of patients with invasive mycoses and to improve the outcome of such infections.

A significant difference was also observed between the TAO groups (P < 0·05). Figure 2 shows the values of the determinations of Th1 cytokine profiles (IFN-γ

and IL-12) in the plasma of normal individuals (smoker, ex-smoker and non-smokers) and patients with TAO (smokers and former smokers). The data results show an increase of these cytokines in the plasma of TAO patients compared with control subjects (P < 0·05 for each comparison). A significant Ruxolitinib purchase difference was also observed between the TAO groups (P < 0·05). Figure 3 shows values of the determinations of Th2 cytokine profiles (IL-4, IL-10, IL-13 and IL-5) in the plasma of normal individuals (smoker, ex-smoker and non-smokers) and patients with TAO (smokers and former smokers). The data results show increased levels of IL-4, IL-5 and IL-13 in the plasma of TAO patients compared with control subjects (P < 0·05 for each comparison). Decreased levels of IL-10 were found in patients with TAO active smokers compared to control individuals and TAO former smokers (P < 0·05 for each comparison). Figure 4 shows the values of the determinations of Th17 cytokine profiles (IL-17 see more and IL-23) in the plasma of normal individuals (smoker, ex-smoker and non-smokers) and patients with TAO (smokers and former smokers). The data results show an increase of these cytokines in the

plasma of TAO patients compared with control subjects (P < 0·05 for each comparison). Because the development and aetiology of TAO have not yet been elucidated, and as the direct action of inflammatory mediators has been observed in the vascular endothelium of TAO patients, in this study we have evaluated some components of the cytokines in the

plasma of TAO patients who presented with acute symptoms. To the best of our knowledge, this is the first complete investigation including cytokines with proinflammatory, Th1, Th2 and Th17 profiles. The precise cause of TAO Ketotifen is still unknown, and different hypotheses have been suggested. A reaction to the constituents of cigarettes is recognized as a factor in the initiation, progression and prognosis of this disease. It is possible that genetic modifications or autoimmune disorders are implicated [5,12,13]. Thus, the strong relationship with smoking seems to involve direct toxicity to the endothelium by certain tobacco products (nicotine) or an idiosyncratic immune response to some agents. Most patients with TAO have hypersensitivity to extracts of tobacco. Peripheral endothelium-dependent vasodilation is impaired in the non-diseased limbs of TAO patients, and this vascular dysfunction may contribute to such characteristics as segmental proliferative lesions or thrombus formation in the peripheral vessels [14]. The immune system seems to play a critical role in the aetiology of TAO.

A number of parallel pathophysiological pathways have been implicated in the pathogenesis of BPH and PCa, including age-related prostate tissue remodelling, hormonal and metabolic alterations, and the previously neglected inflammatory disorder. Recently, PCa and BPH have been considered in the context of local immune reactions and inflammatory response of the prostate, which may also be reflected systemically [2]. The normal, healthy prostate is infiltrated by small numbers of T cells, B lymphocytes, and macrophages, all of which provide physiological

protection to the tissue [3]. BPH, which is stromal hyperproliferation and epithelial overgrowth of the prostrate tissue, is associated with increased leucocyte infiltration [4] relative to the intensity of the inflammation [3]. Several lines of evidence have shown that Small molecule library the prostate tissue in patients with BPH contains diffuse infiltrates of T lymphocytes, predominantly CD4+ cells, in the stroma [5]. Similarly, in PCa, tissue-infiltrating lymphocytes (TILs) have been observed in

and around the cancer tissue [6]. Although Belnacasan purchase previous studies on various cancers have shown that tumour infiltration with TILs is associated with increased survival [7–9], there does not appear to be a correlation between the presence of TILs and survival of patients with PCa. This may be because of the infiltration of regulatory T cells, which negatively correlates with the immune response against cancer [10]. However, Kasic and Viola [11] performed phenotype analysis and showed that TILs of PCa samples were predominantly CD8+ cells. Another possible reason for ineffective surveillance in patients with PCa could be the inadequate expression of cytotoxic molecules, such as perforin (P), in and around the tumour [12]. However, in BPH tissue, P-expressing cells were rare, although the survival of these patients was not affected [12]. Moreover, little is known about the role of NK cells, which are potent effectors of innate immunity

in the first line of tumour defence. Fossariinae P is the primary mediator of short-term cytotoxicity and forms pores in the membranes of target cells (pore-forming molecule). It is accumulated in response to pro-inflammatory cytokines (IL-12, IL-15 and IL-18), stored in the cytoplasmic granules of cells with a cytotoxic phenotype (T lymphocytes, NK cells and NKT cells as a unique subpopulation of T lymphocytes which share common characteristics of T and NK cells), and released upon activation [13–18]. At the ‘cellular synapse’, the released P monomer begins to polymerize in the presence of Ca+ ions and imbeds in the membrane of target cells, forming pores that allow ion exchange. This leads to osmotic imbalance and ultimately, necrosis of the target cell [19].

All conditions were tested in triplicate. Cells were incubated at 37°C and 5% CO2. The efficiency of transduction was confirmed by fluorescence microscopy. A luciferase reporter assay was used as described previously [24, 32] to confirm the ability of the recombinant Tax2 proteins to regulate viral transcription. Cell-free supernatants from Tax-treated PBMCs were harvested at various time-points and assayed for MIP-1α,

MIP-1β and RANTES expression by quantitative enzyme-linked immunosorbent assay (ELISA) (R&D Systems), as described previously [24]. Absorbance values at 490 nm were used to quantify the chemokine levels in

the culture EPZ6438 supernatants from the standard concentration curve and CC-chemokine protein levels were expressed in picograms per millilitre (pg/ml). To determine the activation of the canonical NF-κB pathway, immunofluorescence studies were performed using Tax-treated-PBMCs for an incubation period of 1 and 2 h. Cells were harvested, washed with phosphate-buffered saline (PBS), fixed and cytocentrifuged onto clean glass slides, then permeabilized with 0·3% Triton X-100 (Sigma) and blocked with 5% normal goat serum (Sigma) for 1 h at room temperature. Phosphorylated p65/RelA was detected with phospho-p65/RelA Tamoxifen monoclonal antibodies (mAbs) (diluted at 1:100) followed by FITC-labelled goat anti-rabbit IgG (H + L), F(ab′)2 mAbs (diluted at 1:200) and incubated at dark-room temperature for 1 h. 4′,6-Diamidino-2-phenylindole (DAPI; Sigma) was use to stain the nucleus. Slides were mounted using anti-fade fluorescent mounting very media. Jurkat and MoT cells were used as negative and positive controls. Images were acquired with an Olympus BX51 epifluorescence microscope equipped with an Olympus DP-70 controller digital

camera system and applicable computer capture software (Tokyo, Japan). ImageJ software was used to determine the intensity of cell fluorescence and the non-specific background was subtracted to obtain the corrected total cell fluorescence (CTCF) as integrated density – (area of selected cell × mean fluorescence of background readings) [33]. PBMCs (1 × 106/ml) were stimulated with 100 pM of recombinant Tax proteins and cells were harvested at 1 or 2 h. Nuclear extracts were obtained and tested for activation of p65/RelA and p50 subunits using the TransAM NF-κB DNA-binding ELISA kit (Active Motif, Carlsbad, CA, USA). Briefly, 10 μg of each nuclear extract were incubated in 96-well plates containing a consensus (5′-GGGACTTTCC-3′) binding site for NF-κB.

Serum MMCP-1 has been shown to be a marker for

mucosal mastocytosis and increased gut permeability [32] as well as for mast cell dependent intestinal inflammation [33]. A strong correlation between anaphylactic score and levels of MMCP-1 was found. However, cross-allergy did not reveal any signs of mast cell activation, as the levels of MMCP-1 in animals challenged with cross-reactive legumes were comparable with the levels of immunized, not challenged animals. This suggests GSK-3 phosphorylation that intestinal mast cells are less activated in the cross-allergic reactions observed. It has been reported that food induced anaphylaxis may depend more on macrophages and basophils than on mast cells [34], and more studies are needed to elucidate the roles of macrophages and basophils in cross-allergy. That no cross-reactivity could be observed in the PCA-test may also support the notion that cross-allergic reactions are not mediated through a mast cell dependent pathway. However, because of the functionality of the test, it could also be a reflection of the difference in affinity between epitopes. Two distinct mechanisms have been reported to induce systemic anaphylaxis in the mouse [35]. The classical pathway is mediated by allergen cross linking of IgE bound to the high affinity receptor (FcεRI) on mast cells. The alternative

pathway is thought to involve macrophages, FcγRIII, IgG antibodies and platelet activating factor [36]. A partial inhibition GNAT2 of lupin specific IgG1 by peanut and soy and of fenugreek specific IgG1 by peanut was observed. A role for both IgE and Ku-0059436 cost IgG1 in the cross-allergic responses in mice is therefore possible. Several studies have implied that both the classical and the alternative pathway of food induced anaphylaxis are involved simultaneously in mice, and that abrogation of one pathway only partially abrogates anaphylactic responses [37–39]. Tsujimura

et al. [40] demonstrated that basophils play a crucial role in IgG mediated anaphylaxis in their mouse model. It has also been reported that mast cells contribute to anaphylaxis through both IgE and IgG1, whereas macrophages contribute through IgG1 exclusively. The role of IgG1 in anaphylactic reactions in mice complicates the extrapolation of findings from mouse to man, as IgG-mediated anaphylaxis to food has not yet been described in man. The relevance to human anaphylaxis of the different pathways observed in mice needs to be investigated. Strait et al. have shown that although the IgE pathway is more sensitive and requires lower threshold levels of antigen for full activation, IgG mediated responses can also be severe [36, 41]. Our studies support the involvement of IgG1 in cross-allergy, while we were unable to confirm the involvement of IgE and mast cells.

Background: Worldwide, more people are receiving anti-TNFα for rheumatologic disorders. There have been a small but significant number of reports regarding PD0325901 its relationship with renal disease. Case Report: A 55 year old lady presented in August 2011 with polyarthralgia and diagnosed to have HLA-B27 positive arthritis. She had no evidence of renal disease at initial presentation. She was treated initially with disease modifying drugs including Prednisolone, Methotrexate, Sulfasalazine and Leflunomide. She also had a history of bronchiectasis, multinodular goitre and haemochromatosis. In March 2012 she represented with an exacerbation

of arthritis with anorexia, significant weight loss and uveitis. She was found to have microscopic haematuria and proteinuria with negative autoimmune and vasculitic screens. Her renal biopsy was suggestive of early focal segmental glomerulosclerosis and was started on ACEI. During the course of her therapy she was commenced on Etarnecept initially and later Adalimumab with improvement in her arthritis and uveitis. However she was noted to have episodic recurrent acute elevation of serum creatinine in July 2013 and again in October 2013, each time coinciding with anti-TNFα injection.

Adalimumab treatment was discontinued in view of temporal association with episodic renal dysfunction. Since then her renal functions were stabilized BMS-354825 manufacturer with reduced proteinuria. Conclusions: We presented a case of de novo glomerulonephritis with acute exacerbations related to anti-TNFα

therapy. In most cases, renal condition improves with withdrawal of therapy as is seen in our patient. High index of suspicion is required when patients are receiving these newer products for presence of renal disease. 302 ACUTE KIDNEY INJURY AND ISCHEMIC ACUTE HEPATIC FAILURE AFTER CONSUMPTION OF JAVA BARB FISH GALLBLADDER IN WEST JAVA, INDONESIA M RUDIANSYAH1, RS GONDODIPUTRO2, R BANDIARA2, AH MARTAKUSUMAH2, R SUPRIYADI2, A AFIATIN2 1Division of Nephrology & Hypertension, Department of Internal Medicine, Faculty of Medicine, Universitas Lambung Etofibrate Mangkurat/Ulin Hospital Banjarmasin; 2Division of Nephrology & Hypertension, Department of Internal Medicine, Faculty of Medicine, Universitas Padjajaran/Hasan Sadikin Hospital Bandung, Indonesia Introduction: Fish gallbladder is usually consumed in Asian countries as a traditional medicine. It improves fatigueness, arthritis, and erectile dysfunction. In Tasikmalaya, West Java, Indonesia, people believe if they consume fresh fish gallbladder of Java Barb (Barbonymus gonionotus) or so called “Tawes” will improves their healthy. In some reports, eating java barb can causes systemic toxicities such as acute kidney injury and acute hepatic failure.

The prevalence of IgE sensitisation to A. simplex was 2.0%, 2.2% and 6.6% in blood donors, the unsorted and Phadiatop® positive serum groups respectively. A considerable degree of cross-sensitisation to shrimp and HDM is further suggested. Unspecific binding due to high total IgE or by binding to CCDs seemed to play a minor role. The prevalence of IgE sensitisation to A. simplex appears to be lower in a Norwegian population than in other high fish consuming countries, but might still be overestimated Doxorubicin chemical structure due to cross-sensitisation.

“
“Macrophages respond to their microenvironment and develop polarized functions critical for orchestrating appropriate inflammatory responses. Classical (M1) activation eliminates pathogens while alternative

(M2) activation promotes regulation and repair. M1 macrophage activation is strongly associated with suppressor of cytokine signalling 3 (SOCS3) expression in vitro, but the functional consequences of this are unclear and the role of SOCS3 in M1-macrophage polarization in vivo remains controversial. To address these questions, we defined the characteristics and function of SOCS3-expressing macrophages in vivo and identified potential mechanisms of SOCS3 action. Macrophages infiltrating inflamed glomeruli in a STA-9090 manufacturer model of acute nephritis show significant up-regulation of SOCS3 that co-localizes with the M1-activation marker, inducible nitric oxide synthase. Numbers of SOCS3hi-expressing, but not SOCS1hi-expressing, macrophages correlate strongly with the severity of renal injury, supporting Thalidomide their inflammatory role in vivo. Adoptive transfer of SOCS3-short interfering RNA-silenced macrophages into a peritonitis model demonstrated the importance of SOCS3 in driving production

of pro-inflammatory IL-6 and nitric oxide, while curtailing expression of anti-inflammatory IL-10 and SOCS1. SOCS3-induced pro-inflammatory effects were due, at least in part, to its role in controlling activation and nuclear accumulation of nuclear factor-κB and activity of phosphatidylinositol 3-kinase. We show for the first time that SOCS3 also directs the functions of human monocyte-derived macrophages, including efficient M1-induced cytokine production (IL-1β, IL-6, IL-23, IL-12), attenuated signal transducer and activator of transcription 3 activity and ability of antigen-loaded macrophages to drive T-cell responses. Hence, M1-associated SOCS3 was a positive regulator of pro-inflammatory responses in our rodent models and up-regulated SOCS3 is essential for effective M1-macrophage activation and function in human macrophages. “
“Collectins contribute to host defence through interactions with glycoconjugates on pathogen surfaces.

g., distribution of receptors, cytolytic molecules, secreted soluble factors) found among the three studies were

consistent with each other, confirming the reliability of gene arrays [42-44]. During the early stages of pregnancy, NK cells are the dominant lymphocyte in the decidua, constituting ∼70% of the total lymphocytes. Approximately 90% of dNK cells belong to the CD56brightCD16– immature phenotype [29], called immature dNK (idNK) cells, which are specialized NK cells remarkably distinct from the mature pNK (mpNK) cell subpopulation. These idNK cells function to regulate key developmental processes, including trophoblast invasion and vascular growth [29, 45]. In a previous study we found that both human RXDX-106 purchase and mice dNK cells play a key regulatory role at the maternal–fetal interface by suppressing Th17-mediated Fostamatinib supplier local inflammation, thus promoting immune tolerance [46]. Compared with mpNK cells,

idNK cells show increased expression of several genes, including inhibitory receptors, growth factors, cytokines, chemokines, and cell cycle or proliferation-related proteins [43]. On the other hand, mpNK cells were shown to have increased expression of genes related to activating receptors, costimulatory factors, and chemokines compared with idNK cells. Additionally, we showed that idNK and mpNK cells had different TF profiles; idNK cells are enriched in homeobox TFs, which may contribute to their immaturity; while mpNK cells are enriched in zinc-finger proteins, which may contribute to their cytotoxic function [29]. Hanna et al. performed a microarray analysis Racecadotril on purified dNK cells in order to generate a transcriptional profile in terms of secreted cytokines, growth factors, and chemokines thought to be crucial for placental development [45]. Several growth factor transcripts known to stimulate angiogenesis and act

as endothelial mitogens, including vascular endothelial growth factor and placental growth factor, were highly expressed in dNK cells [45]. These data highlight the superior ability of the dNK over the pNK subpopulation to secrete various mediators important for trophoblast invasion and vascular growth. Additionally, several chemokine transcripts, including Cxcl8, Ccl5, and Cxcl10, were also highly expressed in dNK cells [29, 45]. Reduced trophoblast invasion and vascular growth in the decidua are thought to be a primary defect in pregnancy [47, 48]. These situations can manifest in several different ways including fetal growth restriction, miscarriage, and preeclampsia. Genetic studies suggest that these conditions are linked to the particular combination of KIR receptors expressed on maternal dNK cells and the HLA-C genes expressed by the fetal trophoblast [45, 49].

10 Rag2−/−) are adoptively transferred into lymphopenic hosts that express their cognate antigen, chicken ovalbumin, as a soluble protein in the bloodstream (sOva Rag2−/−). The combination of antigen and lymphopenia results in massive donor T-cell expansion, leading to multiorgan infiltration and lethal autoimmune disease mediated by Th1- and Th17-type effector T cells [14]. To determine whether Th2-type cytokines also play a role in this pathology, we BIBW2992 performed adoptive transfers and measured IL-4 and IL-13 by intracellular flow cytometry. These studies showed that, while unable to produce IL-4, a large fraction

of the donor T cells could produce IL-13 both during the onset (day 3) and peak (day 7) of disease. Many donor T cells were positive for IFN-γ and IL-17, which is consistent with previous work [14, 15], and few were positive for IL-2 (Fig. 1A). Having established that donor T cells produce IL-13 in sOva Rag2−/− Ensartinib purchase hosts, we next asked whether they coexpress other cytokines. Surprisingly, we found that IL-13 often segregated with IFN-γ and IL-17 (Fig. 1B), the signature cytokines of Th1- and Th17-type effectors

[2, 6]. To ask whether IL-13-producing Th1 and Th17 cells can be generated in the absence of lymphopenia or systemic inflammation, we transferred DO11.10 Rag2−/− T cells into congenic, lymphoreplete mice, then immunized with Ova-pulsed antigen presenting cells (APCs). In contrast to sOva Rag2−/− hosts, we could detect donor T cells expressing both IL-4 and IL-13 in these immunized hosts, which demonstrates that our immunization protocol does induce “classical” Selleckchem Fludarabine Th2-type effectors. We could also detect IL-13+ donor T cells coexpressing either IFN-γ or IL-17, which confirms that IL-13-producing Th1 and Th17 cells can be generated in the context of

“protective” immune responses. In fact, on a per cell basis, the percentage of Th1 and Th17 cells producing IL-13 was comparable between immunized and autoimmune sOva Rag2−/− hosts (Fig. 1C and D). It should also be noted that, overall, the percentage of IL-13+ cells was far greater than that of IL-4+, IFN-g+, or IL-17+ cells, which suggests that IL-13 can be produced either alone or in concert with unidentified cytokines. Coexpression of IFN-γ and IL-17 was seen in sOva Rag2−/− hosts but not immunized hosts, which suggests a link to autoimmunity, and coexpression of IL-17A and IL-17F was common to both models (Supporting Information Fig. 2). To ask whether IL-13-producing Th1 and Th17 cells can be generated during polyclonal T-cell responses, we used a model of chemically induced colitis where T cells are primed in response to a range of microbial and self-antigens. First, we determined that, compared to untreated controls, DSS-treated mice had increased numbers of IL-13+ CD4+ TCRβ+ cells within mesenteric lymph nodes (Supporting Information Fig. 3).