, 2010; Kreisel et al., 2011). USA300-related strains were also more prone to spread from the initial infection site and caused more severe infections than HA-MRSA in patients suffering from MAPK Inhibitor Library mw pneumonia with pulmonary emboli (Ganga

et al., 2009; Hota et al., 2011). However, other reports describe better clinical outcomes associated with USA300 infections (Lalani et al., 2008; Moore et al., 2009). Although some studies that reported more positive clinical outcomes with CA-MRSA also describe hypervirulent CA-MRSA trends that merely lack full statistical significance, such as increased risk of being admitted into intensive care (OR = 1.8, P = 0.09) (Popovich et al., 2008). Everolimus Additionally, effective treatment, which is easier to achieve when treating CA-MRSA infections given their inherent susceptibility to clindamycin, tetracyclines, rifampicin and trimethoprim/sulfonamide, can reduce

the severity of CA-MRSA disease outcomes in population-based studies (Bassetti et al., 2011). Unfortunately, this trend of increased antibiotic susceptibility may be diminishing as new reports show increased antibiotic resistance among USA300 isolates, possibly through direct acquisition of resistance determinants from multidrug-resistant HA-MRSA strains (McDougal et al., 2010). Thus, the future clinical outlook appears grim with respect to USA300 infections given their increased prevalence in both hospital- and community-acquired infections, their propensity

to acquire new antibiotic resistance determinants, and the steady decline in positive clinical outcomes associated with USA300 infections. Given the recent impact of USA300 on human health, significant research effort has been exerted to elucidate the source of USA300 success. Here, we review these findings and broadly categorize them into three main classes: (1) newly acquired genes that promote virulence and/or fitness, (2) altered regulation of Carnitine dehydrogenase core genes resulting in elevated virulence and/or fitness, and (3) nonsynonymous mutations in core genes that enhance virulence and/or fitness. Many different lineages of CA-MRSA (USA400, USA1000, and USA1100) cause outbreaks and invasive infections, but in North America, none are as prevalent as epidemic USA300. These clones have acquired many genes in the form of MGEs that may confer a selective advantage over other CA-MRSA strains. Several groups have investigated many of these MGEs with the goal of elucidating factors (if any) that have contributed to the overwhelming success of USA300. USA300 CA-MRSA isolates contain genes encoding enterotoxins K and Q (sek2 and seq2) in a unique pathogenicity island SaPI5 (Diep et al., 2006a). Sek2 and Seq2 are thought to contribute to pathogenesis by stimulating T-cells through binding of the Vβ chain of αβ T-cell receptors.

030 and 0.039, respectively); FEV1/FVC increased by 0.034 and 0.021 per the minor G allele was present. Table 4 indicates the associations between the SNPs in the ALOX5AP and FEV1 or FEV1/FVC. This study is unique because most studies examining associations between genetic variation and diseases, including lung-related diseases, have focused on patient populations rather than healthy population. Healthy population-based studies such as the present one are important because they

may facilitate disease prevention, which is more effective than treating diseases once they have developed. The ALOX5AP gene participates in the 5-LO pathway, which is known GSK3235025 nmr to play a role in several disease processes [20]. The present study analysed the effect of this gene on the lung functions of pulmonary disease-free Koreans and all Korean in cohorts. Several genotypes were found to associate significantly with the baseline lung function FEV1. Interestingly, no SNP was associated with FEV1 in Ansan but there were several identical SNPs, rs10162089, rs3803277 and rs9506352, associated with FEV1 in Ansung and combined data in both healthy and general Gemcitabine supplier population. From that, it was assumed that those SNPs associated with FEV1 affects the lung function level and development of respiratory diseases such as asthma and chronic lung disease may be indirectly

influenced. A previous case–control study revealed that the ALOX5AP gene was not associated with FEV1 in aspirin Dapagliflozin acetylsalicyclic

acid-intolerant asthma [21]. Polymorphism of the ALOX5AP gene promoter was also found not to affect the development of asthma in Australian and Caucasian populations [22, 23]. However, Holloway et al. [24] have identified associations between ALOX5AP SNPs and asthma-related phenotypes such as FEV1, total IgE, atopy and bronchial hyper-responsiveness, although Klostman et al. [25] found that ALOX5AP genetic variation did not affect the response of patients with asthma to montelukast, which is a leukotriene modifier. These two studies did not find an association between rs3803277 and FEV1 or other phenotypes. In contrast, the present study revealed a significant (P < 0.05) association between rs3803277 and FEV1 in general population; this association remained significant after permutation testing. The 5-LO pathway is also associated with chronic rhinosinusitis and various cardiovascular diseases [26]. The polymorphisms at position (-1072)G>A and (-444)A>C of the LTC4 synthase were associated with increased risk of transient ischaemic attack and ischaemic stroke but not associated with asthma and COPD in Danish general population [27]. Helgadottir et al. [28] found two ALOX5AP halotypes, HapA and HapB, which play critical roles in the development of myocardial infarction and stroke.

The DDSTs were performed as described previously [13, 19]. A 0.5 McFarland bacterial suspension was inoculated on a Mueller selleck Hinton agar plate (Eiken Chemical). Antimicrobial disks containing either 30 µg CAZ, 10 µg IPM, 10 µg panipenem, 10 µg meropenem, 10 µg biapenem, 10 µg doripenem or 10 µg tebipenem (Eiken Chemical) were used as substrates. Two disks of an antimicrobial agent were placed at least 30 mm apart on a Mueller Hinton agar plate and a blank or SMA

disk placed either 7, 10, 15, or 20 mm from the antimicrobial disks (measured from center to center). Twenty-five microliters of each metal-EDTA solution was added to a blank disk. After incubation at 35°C for 16–18 hrs, the appearance of a ≥5 mm enhanced zone around the antimicrobial disk near the inhibitor disk was classified as positive (Fig. 1). Using an SMA disk and seven types of metal-EDTA disks, DDSTs were performed for seven MBL producers carrying NDM-1, IMP-1, VIM-2 and JQ1 nmr IMP-11 and three non-MBL producers carrying KPC, CTX-M-2 and chromosomal AmpC (Table 1). CAZ or IPM disks were placed 15 mm from the metal-EDTA disks and the resultant enhancement of the zone of growth inhibition evaluated. Two NDM-1 producers showed negative results when SMA disks were used. However, DDSTs using Mg-EDTA, Ca-EDTA, Co-EDTA or

Cu-EDTA were positive for NDM-1 producers when IPM disks were used. Regarding IMP-1, VIM-2 and IMP-11 producers, Mg-EDTA and Cu-EDTA inhibited all five MBLs in the DDSTs using CAZ. There were no false positive results for the three non-MBL producers. Because P. aeruginosa 7117 was positive only when Mg-EDTA and IPM were used, Mg-EDTA was selected Resminostat for further

studies. First, the appropriate concentration of Mg-EDTA for detecting MBL when a Mg-EDTA disk was placed 15 mm from an IPM disk was evaluated. A. baumannii 7170 carrying blaIMP-1 was negative when 8 mg Mg-EDTA disks were used with IPM disks and positive when 10 mg Mg-EDTA disks were used with IPM disks. Therefore, a disk content of 10 mg Mg-EDTA was selected for the subsequent experiments. Next, the optimal distance between antimicrobial and Mg-EDTA disks was evaluated. K pneumoniae ATCC BAA-2146 was used as a positive control strain for NDM-1 producers, and A. baumannii 7170 as a weak positive control strain for IMP-1 producers. Two strains producing either NDM-1 or IMP-1 were positive when 10 mg Mg-EDTA disks were placed 15 mm away from the IPM disks; however, they were negative when the Mg-EDTA disks were placed 20 mm away from the IPM disks. Therefore, it was decided that the Mg-EDTA and IPM disk would be placed 15 mm apart for the subsequent experiments. To evaluate the efficiency of Mg-EDTA disks, 75 stock cultures carrying the various MBL genes and 25 stock cultures carrying other β-lactamase genes were tested by DDSTs using 10 mg MgEDTA–IPM or MgEDTA–CAZ. Positive results for MgEDTA–CAZ were obtained in 69 test strains (92.

LTD4 is known to prime alveolar macrophages

to produce mediators such as MIP-1α, TNF and NO when stimulated with LPS [35]. In our study, sCD14 production in PBMC-CD14+ cultures was blocked by the co-incubation of LTD4 with the LTRA Montelukast. This observation supports the hypothesis that LTRAs could exert some of their anti-inflammatory effects by inhibiting LPS-induced augmentation of the asthmatic inflammation. This is further supported by previous reports where the LTRA pranlukast was able to suppress NF-κ activation, an intracellular signalling pathway which is also activated by LPS in human monocytes/macrophages as well as by Tcells Talazoparib solubility dmso [51]. In our study, there was a trend towards an increase

in sCD14 production in PBMC-CD14+ LDK378 price cultures following stimulation with LPS and the combination of LPS and LTD4 that, however, failed to reach statistical significance, possibly as a result of a relatively short stimulation interval, as in vivo the maximal sCD14 concentrations were measured 42–44 h after allergen and LPS stimulation [44], respectively. Therefore, we cannot rule out that a more prolonged stimulation of PBMC-CD14+ cultures might have resulted in a significant increase in sCD14 production. In conclusion, kinetic analysis of the local endobronchial sCD14 production suggests that sCD14 concentrations reach their maximum around 42 h after segmental allergen challenge. We provide evidence that LTD4 stimulates sCD14 production in PBMC-CD14+ cultures which could contribute to the proinflammatory potential of this mediator. The leukotriene-receptor antagonist Montelukast is able to block this effect, suggesting that this is indeed a CysLTR-1 mediated effect. As LPS seem to have a protective role in the development of asthma on the one hand [1], possibly related to LPS dose and genetic constellation 4-Aminobutyrate aminotransferase [2, 4], it can aggravate existing asthma

on the other hand [3]. Based on our in vitro findings, it could be speculated that leukotriene-receptor antagonists might be able to block the effects of LPS-induced aggravation of allergic asthma in vivo. “
“Mucosal leishmaniasis (ML) is characterised by severe tissue destruction. Herein, we evaluated the involvement of the IL-17-type response in the inflammatory infiltrate of biopsy specimens from 17 ML patients. IL-17 and IL-17-inducing cytokines (IL-1β, IL-23, IL-6 and TGF-β) were detected by immunohistochemistry in ML patients. IL-17+ cells exhibited CD4+, CD8+ or CD14+ phenotypes, and numerous IL-17+ cells co-expressed the CC chemokine receptor 6 (CCR6). Neutrophils, a hallmark of Th17-mediated inflammation, were regularly detected in necrotic and perinecrotic areas and stained positive for neutrophil elastase, myeloperoxidase and MMP-9.

Each amplified DNA fragment covered the region from the 18th to 172nd of the lipase gene and that from the 541st to 711th of the 16S rRNA

gene, respectively. The annealing temperature of the oligonucletotides for lipase gene is 55°C and that for 16S rRNA is 51°C. The thermal protocol was 95°C for selleck chemicals llc 3  min and then 35 cycles of 95°C for 10  sec and the annealing temperature indicated above for  30 sec and 72°C for 30  sec. Fluorescence was measured at the end of the 72°C step during every cycle. As a control, a reaction mixture without reverse transcriptase was prepared using same protocol. The threshold for fluorescence was properly positioned according to the manufacture’s learn more protocol, and the number of cycles at which fluorescence reached the threshold line was determined. The relative transcriptional level of lipase gene was calculated according to the formula of the ΔΔCt method (26). In order

to comprehensively examine the effect of NaCl on production of extracellular proteins, we cultured two strains, wild-type strain (A. sobria 288 [asp+, amp+]) and two protease gene-deleted mutant strains (A. sobria 288 [asp−, amp−]), in NB (0.5) and NB (3.0) at 37°C for 24  hrs with shaking. We treated these culture supernatants with TCA, and collected and separated the precipitates yielded by SDS-PAGE as described in Materials and Methods. The results are shown in Figure 1. We applied samples of the wild-type strain, which we prepared by culturing in NB (0.5) and NB (3.0), to lanes 1 and 2, respectively. Compared with lane 2, the number of protein bands in lane 1 was small and their density low. We believe that both ASP and AMP were

produced in the wild type culture supernatant in NB (0.5) and that almost all proteins released into the culture supernatant were decomposed by these proteases. In contrast, we prepared the sample for lane 2 from the culture supernatant in NB (3.0). In NB (3.0), production of ASP and Thymidine kinase AMP is repressed (8, 17). Therefore, many proteins in the culture supernatant were not attacked by these proteases. Thus, the number of bands was large and their densities high in lane 2. The above results show that the protease activity of the culture supernatant strongly influences the appearance of protein in it. It is important to eliminate the influence of proteases when analyzing exoproteins released into the milieu from bacteria. We therefore analyzed the exoproteins of a two protease gene-deleted mutant strain (A. sobria 288 [asp−, amp−]).

2,25–27 The selection of appropriate, targeted antimicrobial therapy must accommodate the fact that a variety of Candida species ranging from C. albicans to C. parapsilosis have been recovered from cases of CRMD-related Candida endocarditis. Accordingly, current treatment guidelines15 include the use

of an amphotericin B formulation (e.g. liposomal formulation amphotericin B – 3 to 5 mg kg day−1) with or without 5-flucytosine 25 mg kg−1 qid or an echinocandin agent such as micafungin 100 mg day−1 as primary therapy. With regard to the echinocandins, it is noteworthy that two recent publications19,24 Tamoxifen clinical trial describe the use of these agents in the treatment of Candida endocarditis. Alternative step-down therapy can include fluconazole 400–800 mg daily for stable patients with a susceptible organism and negative blood culture results. Treatment is continued for 4–6 weeks after device removal. In summary, CRMD-associated Candida endocarditis is a rare but potentially life-threatening event, the microbiology can include both common and uncommon Candida BGB324 in vitro species and treatment involves both device removal and well-targeted antifungal therapy. “
“Invasive fungal infections (IFI) lead to morbidity and mortality in neutropenic patients and in allogenic stem

cell transplantation. Serum-based fungal detection assays have limitation of specificity or sensitivity. Studies on fungal DNA detection using real-time PCR in childhood leukaemia are lacking. The aim of this study was to develop sensitive and specific diagnostic tools for IFI in paediatric acute leukaemia patients selleck chemical using real-time PCR.

Of 100 randomised paediatric acute leukaemia patients receiving antifungal prophylaxis with voriconazole/amphotericin B, single peripheral whole blood sample in EDTA was used for Pan-AC real-time PCR assay (detects nine Candida and six Aspergillus species) in patients who failed prophylaxis due to proven, probable, possible or suspected fungal infections. PCR results were retrospectively correlated with clinical profile. Real-time PCR test was positive in 18/29 (62%) patients who failed prophylaxis. The only patient with proven IFI (mucormycosis), real-time PCR assay was negative. Real-time PCR was positive in 2/4 (50%) patients with possible and 16/24 (66.6%) suspected IFI and 5/10 (50%) patients with pneumonia. By applying method A/B, sensitivity and positive predictive value could not be commented due to unproven Aspergillus or Candida infections; specificity and negative predictive values (NPV) were 41% and 100% respectively; by method C (included episodes of possible IFI as true positive), sensitivity, specificity, PPV and NPV were 50%, 36%, 11% and 81% respectively. In those with suspected IFI, 8/24 (33.

Pathological studies disclosed a small brain with hypomyelination and secondary hypoxic-ischemic changes. Neuronal

heterotopia in the white matter and leptomeningeal glioneuronal heterotopia indicated a neuronal migration disorder. The liver showed fibrosis and cholestasis. The thymus and adrenal glands were hypoplastic. Array comparative genomic hybridization (CGH) analysis suggested that the deletion was a genomic rearrangement in the 90-kb span starting in DXS1357E/BACP31 exon 4 and included ABCD1, PLXNB3, SRPK3, IDH3G and SSR4, ending in PDZD4 exon 8. Thus, the absence of ALDP, when combined with defects in the B-cell antigen receptor associated protein 31 (BAP31) and other factors, severely affects VLCFA metabolism on peroxisomal functions and produces ZS-like pathology. “
“C. Voigt, C. K. Donat, W. Hartig, A. Förschler, M. Skardelly, D. Stichtenoth, T. Arendt, J. Meixensberger and M. U. Schuhmann selleck PLX4032 research buy (2012) Neuropathology and Applied Neurobiology38, 354–366 Effect of leukotriene

inhibitors on evolution of experimental brain contusions Aims: Leukotriene levels increase in cerebrospinal fluid (CSF) following controlled cortical impact (CCI) injury in rats. We investigated the impact of two different leukotriene inhibitors in the CCI model on CSF leukotriene levels, brain water content (BWC), brain swelling (BS) contusion size and cellular response. Methods: 134 male Sprague Dawley rats were investigated at 4, 24 and 72 h after CCI for CSF leukotriene levels

and BWC/BS, lesion size in T2-weighted magnetic resonance imaging and immunohistochemistry. Animals Idoxuridine received vehicle, MK-886, an inhibitor of 5-lipoxygenase activating protein, or Boscari®, a mixture of boswellic acids, acting as competitive nonredox 5-lipoxygenase inhibitors before trauma and then every 8 h until sacrifice. Results: The intracranial pressure (ICP) was unaffected by treatment. Boscari treatment reduced CSF leukotriene C4 increase by −45% at 4 h (P < 0.03) and increase of BWC and BS by 49% (P < 0.05) and −58% at 24 h. Treatment with both substances showed a reduction of lesion volume at 72 h by −21% (P < 0.01) in T2-weighted magnetic resonance imaging, which was reflected in a smaller lesion area determined from a NeuN labelled section (−17% to −20%, P < 0.05). Triple immunofluorescence and Fluoro-Jade B staining showed rarefaction of neurones, glia and vasculature in the contusion core, whereas in the pericontusional zone astro- and microglia were upregulated in the presence of dying neurones. Treatment resulted in an improved survival of NeuN labelled neurones in the pericontusional cortex (+15% to +20%, P < 0.05). Conclusions: Leukotriene inhibition should be further investigated as therapeutic option to counteract secondary growth of traumatic brain contusions and to possibly improve pericontusional neuronal survival.

Amplitude of the Nc is thought to reflect the

amount of attention directed at a visual stimulus and is related to autonomic arousal (Reynolds & Richards, 2005). These findings suggest that gaze and head orientation direct infants’ attention buy Alisertib toward peripheral targets, thus facilitating processing of gaze-cued objects. Uncued objects, in contrast, seem to be encoded less effectively and require further processing when they are presented again, eliciting increased brain responses and visual examination. To sum up, even though infants’ overt “gaze” following is affected by the status of a person’s eyes only by the end of the first year, eye gaze serves as an attention-directing cue from birth on, influencing infants’ object

processing by 4 months of age. There is strong evidence that eye gaze shifts in the absence as well as in the presence of congruent changes in head orientation affect infants’ processing of novel objects (Hoehl, Wahl, Michel, & Striano, 2012; Reid & Striano, 2005; Reid et al., 2004; Theuring, Gredebäck, & Hauf, 2007; Wahl et al., 2012). However, do isolated head orientation cues also influence infants’ object processing? mTOR inhibitor Can this information even override incongruent gaze cues? These questions bear importance for our understanding of the early development of social attention cueing mechanisms. According to an influential model on the direction of attention through social cues, separate but interconnected neuronal populations process eye gaze, head orientation, and body orientation (Perrett & Emery, 1994; Perrett, Hietanen, Oram, & Benson, 1992). Investigating the effects of isolated eye gaze and head orientation cues will provide information on whether these cues are processed isolated from each other or in conjunction in Methocarbamol early development and whether both are equally effective

in influencing young infants’ object processing. Thus, the aim of the current study is to disentangle the effects of eye gaze and head orientation on 4-month-olds’ processing of objects using eye tracking and ERPs. We present infants with isolated eye gaze or head orientation cues in a between-subjects design. We predict that infants will direct more visual attention and neural resources to uncued objects in the eye gaze condition when they are presented a second time, thus replicating earlier work. We tentatively predict that infants will also follow the direction of the head turn alone, which may consequently affect object processing.

Interestingly, there is some evidence describing the conversion of murine CD4+CD25+FOXP3+ Treg cells into CD4+CD25+FOXP3- T cells as a result of FOXP3 downregulation, thus subverting Tregs to T effector and predisposing autoimmunity [34, 35]. Indeed, chronic inflammation seen in CVID disease might create a milieu in which activation

of effector T cells may cause downregulation of FOXP3 via production of inflammatory cytokines, thus alter Tregs’ proportions and consequently increase the risk of autoimmunity [17]. However, more studies are needed to support this idea. Our findings in this study indicate that both CTLA-4 and GITR mRNA levels are decreased in CVID patients compared to the control group. This is the first time that

CTLA-4 and GITR genes are evaluated at mRNA level in CVID patients. Only one study JAK inhibitor by Yu et al. showed that the GITR molecule expression is attenuated at protein level (using MFI by flow cytometric analysis) in CD4+CD25highCD127low Tregs from CVID patients with autoimmunity comparing those without autoimmunity and also healthy BGB324 controls [21]. Several mechanisms for Tregs-mediated immune suppression have been described in which both surface markers (e.g. CTLA-4, GITR, LAG-3) and soluble cytokines (e.g. IL-10, TGF-β and IL-35) have been implicated [8-10]. However, the role of soluble factors is still controversial and cell–cell contact has also been

considered as a major aetiology [8-10]. The CTLA-4 and GITR molecules are constitutively expressed at high levels on Tregs’ surfaces. The main role of CTLA-4 molecule is to compete with CD28 molecule for CD80/CD86 markers on dendritic cells (DCs) and thus restraining the effector T cell activation [8, 36]. Negative signal transduction of Tregs by CTLA-4 to DCs can convert them to tolerogenic DCs [37]. During the effector phase of an immune response, the GITR molecule promotes Tregs’ activation and proliferation, which restrict uncontrolled immune cell activation [38, 39]. Hence, it is possible that changes in CTLA-4 and GITR expression together with downregulation of FOXP3 protein might MYO10 account for Tregs’ dysfunction observed in CVID patients. It is possible that ICOS has the same costimulatory role in Treg activation (like conventional T cells) and genetic defect in ICOS gene has been reported to be associated with susceptibility to CVID and defective Treg function [40]. Therefore, evaluating the expression of ICOS might provide additional data in pathogenesis of CVID and should be considered in future studies. Furthermore, recent study reported that Th17 populations differentiated in vitro from natural naive FOXP3+ Tregs, which should be investigated in another study via evaluation of IL-17-producing cells in CVID patients [41].

23,111 Danger and stress selleck chemicals llc signals following allergen encounter or parasite invasion can invoke danger-associated molecular patterns (DAMPs) such as ATP.113–115 ATP, in addition to TLR signalling, can potently activate the inflammasome leading to IL-1β processing, which has been shown by several groups to enhance Th2 effector responses.89,116–118 Interestingly, blood dwelling schistosomes posses ATP-catabolizing enzymes on their tegument surfaces that breakdown ATP to adenosine, potentially interfering with this pathway.119 Following differentiation, Th2 cells are distinguishable from

Th1 cells by more than just cytokine gene activation. For example, Th2 cells lose the ability to sustain calcium flux 120 resulting in reduced tyrosine phosphorylation.121 Th2 cells also have an unconventional synapse, relative to Th1 and naive T cells, and fail to form a ‘bulls-eye’ structure.122 These apparent differences may be because of reduced CD4 and increased CTLA-4 expression, as suggested by others.123 The consequences of these structural buy Regorafenib differences between Th1 and Th2 cells are unclear. Unlike IFN-γ, which is secreted directionally in the immunological synapse, IL-4 can be secreted multi-directionally influencing many surrounding cells.124,125 Whether this is a result of altered

synapse formation or not has not been reported. Also, whether IL-5 and IL-13 are indiscriminately secreted multi-directionally within the reactive lymph node has not been reported. The precise activation

signals received by differentiated Th cells, stimulating their effector function are rather vague. For example it may not be desirable for a Th2 cell, or Th1, Th17 or Th9 cell, to release their payload Megestrol Acetate of potent cytokines, beyond polarizing IL-4, in the case of Th2, within the T-cell zones of lymphoid tissue. Therefore, restricted re-activation via peptide-loaded MHC-II-expressing cells or other activating signals at the site of infection, allergy or action must take place. What these additional signals are is surprisingly unclear. Following Th2 differentiation, chromatin remodelling at conserved non-coding sequence (CNS)-1, DNase I hypersensitivity (DHS) site, CNS-2 and the conserved intron 1 sequence of IL-4 (CIRE) in the il4 locus facilitates rapid cytokine transcription.126–128 Poised in such a state, it may only require a ‘tickle’ to induce translation and secretion of these cytokines. An elegant study by Mohrs et al.,129 using a dual reporter system to identify transcription and secretion of IL-4, discovered that although IL-4 was transcribed in lymphoid and non-lymphoid tissue, secretion was only observed in non-lymphoid tissue upon antigen encounter. This study is in slight contradiction to a recent paper from the same group identifying the widespread influence of IL-4 in the reactive lymph node.