We are thankful to all the members of our local committee, especially Ursula Goodenough for her support. We are highly indebted to Don Ort and his program committee for the excellent program they have brought before us. Appendix Congress co-chairs Robert E. Blankenship (Washington University in Saint Louis) and Donald R. Ort (University of Illinois, Urbana-Champaign & USDA/ARS). Program committee Donald Ort (chair; University of Illinois—Urbana-Champaign & USDA/ARS), Lisa Ainsworth (University of Illinois—Urbana-Champaign),

Carl Bernacchi (University of Illinois—Urbana-Champaign), Thomas Brutnell (Donald Tipifarnib price Danforth Plant Science Center), Evan De Lucia (University of Illinois—Urbana-Champaign), Andrew Leakey (University of Illinois—Urbana-Champaign), Stephen Long (University of Illinois—Urbana-Champaign), Himadri Pakrasi (Washington University in Saint Louis), Klaus Schulten

(University of Illinois—Urbana-Champaign), Michael Wasielewski (Northwestern University, Evanston), and Colin Wraight (University of Illinois—Urbana-Champaign). Local arrangements and coordinating committee Robert Blankenship (chair; Washington University in St. Louis), Jason Cooley (University of Missouri, Columbia), Susan Dutcher (Washington University selleckchem School of Medicine), Ursula Goodenough (Washington University in St. Louis), Govindjee (University of Illinois—Urbana-Champaign), Chad Henry (Washington University in St. Louis), Susan Martino-Catt (Monsanto Corporation), Kaslina Love-Mosely (Washington University in St. Louis), Elizabeth Dorland (Washington University in St. Louis), Erin Plut (Washington University in St. Louis), and Judy Musick (Washington University in St. Louis). Reference Foyer CH (2006) Photosynthesis coming of age to meet the needs of the 21st century: an invitation to the 14th international congress on photosynthesis research in 2007. Photosynth Res 89:3–6CrossRef”
“Prologue The interview presents an overview of Benson’s undergraduate and graduate education, his experiences as a young Ph.D. and the eight years he spent as a researcher in Melvin Calvin’s laboratory when the photosynthetic carbon

cycle was worked out. It becomes apparent that Benson’s contributions to elucidating the cycle are manifold. They include bringing expertise Olopatadine in carbohydrate chemistry and experience with radioactive carbon to Calvin’s research group; introduction of experimental approaches such as the “lollipop,” radioautography and procedures for degrading intermediates of the cycle; identification of 3-phosphoglyceric acid as the first stable product formed in short exposure experiments with 14CO2 (with Calvin); and discovery of ribulose-1,5-bisphosphate, the elusive intermediate that enabled the group to formulate the cycle—a concept that Calvin had long championed as the mechanism of CO2 fixation in photosynthesis. Benson describes first-hand how the experiments were carried out and what life in the Calvin laboratory was like.

Biochem Biophys Res Commun 2004,325(2):612–618.PubMedCrossRef 32. Lopez B, Aguilar D, Orozco H, Burger M, Espitia C, Ritacco V, Barrera L, Kremer K, Hernandez-Pando R, Huygen K, et al.: A marked difference in pathogenesis and immune response induced

by different Mycobacterium tuberculosis genotypes. Clin Exp Immunol 2003,133(1):30–37.PubMedCrossRef 33. Mawuenyega KG, Forst CV, Dobos KM, Belisle JT, Chen J, Bradbury EM, Bradbury AR, Chen X: Mycobacterium tuberculosis functional network analysis by global subcellular protein profiling. Mol Biol Cell 2005,16(1):396–404.PubMedCrossRef 34. Jucker M, Tian M, Norton DD, Sherman C, Kusiak JW: Laminin alpha 2 is a component of brain capillary basement membrane: reduced expression in dystrophic dy mice. Neuroscience 1996,71(4):1153–1161.PubMedCrossRef Selleck PF2341066 35. Powell SK, selleckchem Kleinman HK: Neuronal laminins and their cellular receptors. Int J Biochem Cell Biol 1997,29(3):401–414.PubMedCrossRef 36. Av-Gay Y, Everett M: The eukaryotic-like Ser/Thr protein kinases of Mycobacterium tuberculosis. Trends Microbiol 2000,8(5):238–244.PubMedCrossRef 37. Prisic S, Dankwa S, Schwartz D, Chou MF, Locasale JW, Kang CM, Bemis G, Church GM, Steen H, Husson RN: Extensive phosphorylation with overlapping specificity by Mycobacterium tuberculosis serine/threonine protein kinases. Proc Natl

Acad Sci USA 107(16):7521–7526. 38. Perez J, Garcia R, Bach H, de Waard JH, Jacobs WR Jr, Av-Gay Y, Bubis J, Takiff HE: Mycobacterium tuberculosis transporter MmpL7 is a potential substrate for kinase PknD. Biochem Biophys Res Commun 2006,348(1):6–12.PubMedCrossRef 39. Greenstein AE, MacGurn JA, Baer CE, Falick AM, Cox JS, Alber T: M. tuberculosis Ser/Thr Protein Kinase D Phosphorylates an Anti-Anti-Sigma Factor Homolog. PLoS Pathogen 2007,3(4):e49.CrossRef 40. DeMaio J, Zhang Y, Ko C, Young DB, Bishai WR: A stationary-phase stress-response sigma factor from Mycobacterium tuberculosis. Proc Natl Acad Sci USA 1996,93(7):2790–2794.PubMedCrossRef why 41. Geiman DE, Kaushal D, Ko C, Tyagi S, Manabe

YC, Schroeder BG, Fleischmann RD, Morrison NE, Converse PJ, Chen P, et al.: Attenuation of late-stage disease in mice infected by the Mycobacterium tuberculosis mutant lacking the SigF alternate sigma factor and identification of SigF-dependent genes by microarray analysis. Infect Immun 2004,72(3):1733–1745.PubMedCrossRef 42. Jain SK, Paul-Satyaseela M, Lamichhane G, Kim KS, Bishai WR: Mycobacterium tuberculosis invasion and traversal across an in vitro human blood-brain barrier as a pathogenic mechanism for central nervous system tuberculosis. J Infect Dis 2006,193(9):1287–1295.PubMedCrossRef 43. Barthe P, Mukamolova GV, Roumestand C, Cohen-Gonsaud M: The structure of PknB extracellular PASTA domain from mycobacterium tuberculosis suggests a ligand-dependent kinase activation. Structure 2010,18(5):606–615.PubMedCrossRef 44.

Statistical analysis Statistical significance was determined using a two-tailed paired Student’s t-test. The results were considered statistically significant with P ≤ 0.05 (*) and P ≤ 0.001 (**). Acknowledgements We would like to thank Dr. Steen for providing the Lactococcus lactis subsp. cremoris strain MG1363. This work was supported in part by National Protein Tyrosine Kinase inhibitor Institutes and Health Grant AI50666 and by a research grant (RFDG) from the West Virginia University Research and Graduate Education (to S. L.). H. Oliver-Kozup was supported by a grant from the West Virginia Graduate

Student Fellowship in Science, Technology, Engineering and Mathematics (STEM). Confocal microscopy experiments were performed in the West Virginia University Microscope Imaging Facility, which is supported in part by the Mary Babb Randolph Cancer Center and NIH grant P20 RR016440. We would like to acknowledge the assistance of the West Virginia Selleckchem CHIR99021 University Flow Cytometry core facility which was supported in part by a grant P30 RR032138 from the National Institutes of Health. The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the National Institute of Occupational Safety and Health. Electronic supplementary material Additional file 1: Figure S1. Biofilm formation by the isogenic wild-type and scl1 -inactivated GAS strains. The figure

shows gallery views and X-Y orthogonal Z-stack views of GFP-expressing GAS biofilms at 24 h rendered by confocal laser scanning microscopy (CLSM). Figure S2. Biofilm formation by the wild-type and Scl1-expressing L. lactis strains. The figure shows gallery views and X-Y orthogonal Z-stack views of GFP-expressing L. lactis biofilms at 24 h rendered by CLSM. (PDF 2 MB) References 1. Conley J, Olson ME, Cook LS, Ceri H, Phan V, Davies HD: Biofilm formation by group a streptococci: is there a relationship with treatment failure? J Clin

Microbiol 2003,41(9):4043–4048.PubMedCrossRef 2. Ogawa T, Terao Y, Okuni H, Ninomiya K, Sakata H, Ikebe K, Maeda Y, Kawabata S: Biofilm formation or internalization into epithelial cells enable see more Streptococcus pyogenes to evade antibiotic eradication in patients with pharyngitis. Microb Pathog 2011,51(1–2):58–68.PubMedCrossRef 3. Boles BR, Thoendel M, Singh PK: Genetic variation in biofilms and the insurance effects of diversity. Microbiology 2005,151(Pt 9):2816–2818.PubMedCrossRef 4. Lauderdale KJ, Malone CL, Boles BR, Morcuende J, Horswill AR: Biofilm dispersal of community-associated methicillin-resistant Staphylococcus aureus on orthopedic implant material. J Orthop Res 2010,28(1):55–61.PubMed 5. Kaplan JB, Meyenhofer MF, Fine DH: Biofilm growth and detachment of Actinobacillus actinomycetemcomitans . J Bacteriol 2003,185(4):1399–1404.PubMedCrossRef 6.

However, apart from the stated advantages, biological synthesis suffers from poor mono-dispersity, random aggregation, non-uniform shapes, problems in scale-up, etc. [13]. Torin 1 clinical trial Though, in recent times, many organisms have been reported to produce nanoparticles, scientific understanding on the mechanism and the machinery related to its production is still in its infancy. Therefore, there is a need to improve upon this green synthesis process with an aim to understand the underlying mechanism

and design a working prototype for biomimetic production of Au NPs. These nanoparticles, upon being adhered to a matrix, may serve as a better catalyst than bulk metal due to greater accessibility to surface atoms and low coordination number especially in the case of water treatment. Among several water pollutants, nitroaromatic compounds are considered as the most toxic and refractory pollutants, of which the permissible range is as

low as 1 to 20 ppb. However, these are common in production of dyes, explosives and pesticides among many others; thus, their industrial production is considered as an environmental hazard [14]. Upon being released into the environment, these nitrophenols pose significant click here public health issues by exhibiting carcinogenic and mutagenic potential in humans [15]. Normally, it takes a long time for degradation of nitrophenols in water which poses considerable risk if it seeps into aquifers along with the groundwater. These nitrophenols tend to

get accumulated in deep soil and stays indefinitely. Although several water treatment methods are available like chemical precipitation, ion exchange adsorption, filtration and membrane systems, they are slow and non-destructive. Therefore, there is a need to remove these highly toxic compounds with efficient catalytic systems. Generally, nanoparticles are immobilized onto supporting materials like silica, zeolites, resins, alumina, microgels, latex, etc. which are inert to the reactants and provide Tyrosine-protein kinase BLK a rigid framework to the nanoparticles. The gold-supported catalysts can then be used to carry out partial or complete oxidation of hydrocarbons, carbon monoxide, nitric oxide, etc. [16]. In a recent study, Deplanche et al. [17] showed coating of palladium followed by gold over Escherichia coli surface in the presence of H2 to produce biomass-supported Au-Pd core-shell-type structures and subsequent oxidation of benzyl alcohol. Likewise, we believe that bacterial biomass is essentially carbonaceous matter which can be used to serve as a matrix for preparing a heterogeneous catalyst with the incorporation of nanoparticles. With this aim, we utilized E. coli K12 strain to check its potential for producing Au0 from AuCl4  −. This strain has been known for its reduction activity as shown with bioremediation studies [18, 19].

However, in combination

with CCR7 downregulation, CXCR5 expression enables the TFH cells to migrate into B-cell follicles in a CXCL13-dependent manner. This process assists the antigen-specific B cells to mount a GC response and to promote the selection of B cells expressing high-affinity antibodies in the GC environment [2, 35, 36]. Neither IgG1+ Venetoclax in vitro memory B cells nor GC B cells are generated in CD40-deficient mice after immunization with a TD antigen, NP-chicken gamma globulin (CGG), or in wild type mice immunized with a T-cell independent (TI) antigen, NP-Ficoll [2]. These results indicate that the development of both GC-dependent and -independent IgG1+ memory B cells requires classical T-cell help. B cells also receive innate nonclassical help from natural killer T (NKT) cells [38], although both GC-dependent and -independent memory B cells develop normally in mice lacking NKT cells [2]. However, GC-dependent and -independent memory B cells are distinct with respect to their dependence on TFH help for their generation and maintenance. We showed in a recent study that the loss of TFH

cells caused by T-cell specific deletion of Bcl6 resulted in complete absence of GCs for at least 40 days [2]. However, total numbers of memory B cells were reduced only about twofold in the absence of TFH cells. This reduction resulted predominantly from the loss of mutated Selleckchem PD-1/PD-L1 inhibitor high-affinity memory B cells, consistent with the notion that

the generation of these cells significantly relies on TFH cells. Significantly, unmutated memory B cells still developed upon conditional deletion of Bcl6 in both either B and or T cells, demonstrating the existence of a TD memory B-cell developmental pathway independent of GCs and TFH cells. Whether naïve B cells are intrinsically programed for recruitment into either the GC-independent or GC-dependent pathway, or can enter either pathway depending on signals received upon activation, remains to be explored. Clearly, both pathways require TD antigenic Unoprostone stimulation. However, the processes following initial B-cell activation are dynamic and involve sequential cellular interactions of different duration [39], which would provide ample opportunities for activated B cells to branch out into alternate differentiation pathways. As discussed above, the polarization of antigen-specific CD4+ T cells into effector Th-cell populations is completed within 3 days during the DC priming period [12]. Based on our study, antigen-binding IgG1+ B cells with a memory B-cell gene expression signature appear at around day 3 after immunization [2].

Conventional B-2 cell-derived plasma cells are surface Ig negative, CD19low/negative and express high levels of the plasma cell marker find more CD138 and slightly higher level of CD43 than B-1 cells (Fig. 5 and 40). BM B-1 cells, >80% of which spontaneously secrete IgM in vitro (Fig. 4C), are surface IgM+IgDlow/negative, and express relatively high levels of CD19 but are CD138− (Figs. 2, 3, 5). Our data are consistent with earlier reports on the phenotype of IgM-secreting B cells 25, 33 and through the use of the allotype chimeras we now identify these BM cells

unequivocally as B-1 cells (Figs. 3 and 4). In addition, as we show here (Figs. 1 and 4), these cells produce antibodies that recognize influenza virus, a specificity we have previously linked to B-1 cell-derived antibodies 5, 26, 27. Staining with antibodies recognizing a B-1a cell-specific Ig-idiotype (T-15) binding to phosphorylcholine, as well as staining with phosphatidylcholine-containing liposomes identified small numbers of BM B-1 cells (data not shown), further confirming their similarity to known B-1 cells with regard to specificity. Notably, these Opaganib mouse cells are distinct from the IgMloIgDhi

sinusoidal BM B cells, which were described recently as rapid IgM secreters following challenge with blood-borne T-independent antigens 42. FACS-sorting experiments did learn more not reveal significant spontaneous IgM secretion among IgMloIgDhi B cells in our

non-challenged mice (Fig. 2). In contrast to BM and spleen, PerC B-1 cells from BALB/c mice or from allotype chimeras were not significant sources of spontaneous IgM secretion (Figs. 1 and 4). Thus, our data are consistent with several in vivo studies that indicated the inability of PerC B-1 cells to produce natural IgM 33, 36, 37. It is remarkable, however, that PerC B-1 cells secrete or shed small amounts of IgM, resulting in large numbers of pinhead-size ELISPOTs (Fig. 1), also noted by others 31, 32, without significant amounts of secreted product amassing in the culture supernatants (Figs. 1 and 3). Such “leakiness” of B cells was not noted for cells harvested from any other tissue, for example the PLNs (Fig. 1). This might explain the apparent discrepancies in the literature regarding IgM secretion by PerC B-1 cells 31–37. Counting of these very small dots by PerC B-1 cells, might lead to an over-estimation of the ability of these cells to secrete significant amounts of natural IgM.

Furthermore, AnnexinV stainings of splenic B cells one day after setting up the in vitro cultures revealed that in contrast to pre-B cells, B cells did not respond to overexpression of Pim1 by increased survival (Fig. 5E). We conclude that overexpression of Pim1 and Myc does not induce ex vivo isolated splenic or peritoneal CD19+ sIgM+ immature or mature B cells to long-term polyclonal proliferation, or selective survival and extended proliferation in the

absence or presence of polyclonal B-cell stimulators. Our experiments presented in this paper describe the effect of the inducible learn more single or double overexpression of the proto-oncogenes Pim1 and Myc in mouse B-lymphocytes at different stages of development, starting at the DJH/DJH-rearranged pre-BI cell stage 1. Many experiments studying the effect of proto-oncogenes on hematopoietic cells have been done using transgenic mice, also in the case of Pim1 and Myc 18. These mice express the transgenes under the control of the μ enhancer of the immunoglobulin heavy chain (Eμ), which is expressed already at a very early stage of B-cell development. The limitation of such transgenic mice is that if the team play

of the transgenic proto-oncogenes leads to a block in differentiation at an early stage of cell differentiation (as it is the case in these Eμ Pim1/Myc transgenic mice), it is not possible to study effects of the proto-oncogenes on later differentiation stages of the cells using these mice. To circumvent this, we used Sirolimus cost an inducible system to overexpress the two proto-oncogenes, which allowed us to evaluate the effect of proto-oncogene overexpression at different stages of maturation. In the experiments presented here, we have used retroviral vectors to overexpress the proto-oncogenes in B-lymphocytes under the control of a doxycycline-inducible promoter. Retroviral vectors are known to induce transformations by themselves by activating surrounding host genes with their LTR promoters and enhancers. Hence,

we used self-inactivating vectors. It can be expected that three subsequent transductions, performed with the pre-BI cells, have generated a genetically heterogenous collection of transduced cells with differential inducibility of Pim1 and Myc. As one example, such transgenetic heterogeneity might well be the reason why only a fraction of the Pim1/Myc-double-transduced Cepharanthine pre-BI cells initiate proliferation upon proto-oncogene induction, probably either due to inactivation of a transgene or inappropriate overexpression levels of the transgene(s). In spite of these disadvantages, the results of our experiments show that retroviral vectors allow the rapid testing of different combinations of proto-oncogenes in our pre-BI cell lines and their differentiated descendants. Our cell cycle analyses with the Myc-single- and the Pim1/Myc-double-overexpressing pre-B cells show an increase of the frequency of cells in cell cycle.

fumigatus. “
“Dermatophytoses are a widespread problem worldwide. Textiles in contact with infected skin can serve as a carrier for fungus propagation. Hitherto, it is unknown, whether

antifungal textiles could contribute in controlling dermatophytes e.g. by disrupting the chain of infection. Testing of antimicrobial fabrics for their antifungal activities therefore is a fundamental prerequisite to assess the putative clinical relevance of textiles for dermatophyte prevention. Fabrics finished with either didecyldimethylammonium chloride (DDAC), poly-hexamethylenbiguanide, copper and two silver chloride concentrations were tested for their antifungal activity against Trichophyton rubrum, selleck kinase inhibitor Trichophyton mentagrophytes and Candida albicans. To prove dermatophyte susceptibility towards the textiles, swatches were subjected to DIN EN 14199 (Trichophyton sp.) or DIN EN ISO 20743 (C. albicans) respectively. In addition, samples were embedded, and semi-thin sections were analysed microscopically. While all samples showed a clear inhibition of C. albicans, activity against Trichophyton sp. varied significantly: For example, DDAC completely inhibited T. rubrum growth, whereas T. mentagrophytes growth remained unaffected even in direct contact

Selleck DZNeP to the fibres. The results favour to add T. mentagrophytes as a test organism in textile dermatophyte efficacy tests. Microscopic analysis of swatches allowed detailed evaluation Galeterone of additional parameters like mycelium thickness, density and hyphae penetration depth into the fabric. “
“Mucormycosis, previously termed as zygomycosis, is caused by fungi belonging to the order Mucorales and is a very severe disease in immunocompromised patients with an often unfavourable

outcome. Given the high morbidity and mortality of mucormycosis, establishing a timely diagnosis followed by immediate treatment is of major importance. As randomised clinical trials are lacking, we present our current diagnostic and treatment pathways for mucormycosis in the immunocompromised host. Due to the difficulty to distinguish mucormycosis from other filamentous fungi, mucormycosis always has to be considered as differential diagnosis in predisposed patients. Diagnostic procedures comprise imaging, microscopy, culture and histopathology and need to be rigorously used. In patients with a high suspicion of mucormycosis, e.g. reversed halo sign on computed tomography scanning, our approach combines liposomal amphotericin B (LAmB) with surgical debridement. In light of the rapid deterioration and poor prognosis of these patients, we prefer a daily dose of LAmB of at least 5 mg kg−1 despite nephrotoxicity. In patients with stable disease we switch to posaconazole 200 mg four times per day. In case of progression antifungal combination is an option.

In line with this hypothesis, the IgM released from CpGPTO-stimulated B cells (14·6 ± 12 μg/ml) displayed unselective binding specificity, e.g. reactivity to lipopolysaccharide, pneumococcal polysaccharide, double-stranded DNA, 5-Fluoracil price single-stranded DNA or tetanus toxoid (Fig. 6b). To investigate

whether CpGPTO binds to autoantigens, we incubated HEp2G cells with supernatants from CpGPTO- or CD40L/rhIL-4-treated B cells or intravenous immunoglobulin G. Immunofluorescence microscopy showed binding of CpGPTO-induced immunoglobulin with a faint, mainly cytoplasmic staining pattern suggestive of low-degree autoreactivity (Fig. 6c). Hence, CpGPTO might preferentially target B cells expressing potentially polyreactive

IgM, which might belong to the IgM memory pool.[17] In B cells, internalization of antigen is mediated by the BCR. Recent studies suggested that physical linkage of a BCR antigen to a stimulatory nucleic acid represents the most efficient means to induce B-cell activation via TLR9.[9, 23, 24] This prompted us to ask whether CpGPTO trigger receptor selleck compound revision by simultaneously engaging BCR and TLR9 signalling in a B-cell subfraction. Notably, unmodified (phosphodiester) CpG ODN (CpGPO) lack mitogenicity (Fig. 7a), but the stimulatory activity of CpGPO was coupled to microspheres additionally Ribonucleotide reductase carrying a BCR stimulus [anti-human immunoglobulin F(ab′)2] (Fig. 7b). However, physical linkage of ODN did not waive the requirement for the TLR9-specific CpG-motif: F(ab′)2-coupled microspheres failed to induce proliferation in the absence of CpGPO or when CpGPO was substituted by a control GpCPO or a poly(T)2o-ODN (Fig. 7c). Next, we asked whether CpGPTO use BCR-dependent signalling. To answer this question, we stimulated B cells with CpGPTO in the presence or absence of inhibitors selectively targeting tyrosine kinases typically recruited upon BCR activation. In support of our hypothesis we found that CpGPTO-triggered B-cell proliferation was partially inhibited by the syk

kinase inhibitor R406 in a concentration-dependent manner (Fig. 7d). By contrast, proliferation was enhanced by 20 ± 0·6% when B cells were pretreated with the lyn inhibitor SU6656 (Fig. 7e), a finding well compatible with hyper-responsiveness of lyn–/– B cells.[25, 26] We concluded that, first, syk and lyn kinases participate in CpGPTO-mediated B-cell activation, and, second, CpGPTO either directly stimulate the BCR or bypass BCR signalling by recruiting molecules associated with proximal BCR signalling. To further investigate this question we sought to perform CpGPTO stimulation in the absence of the BCR. To this end we used plasmacytoid dendritic cells because they are characterized by TLR9 and a BCR-like signalosome.

4,5 Interleukin-21 potently stimulates the differentiation of B cells into antibody-forming cells. Moreover, IL-21 synergizes with IL-15 in proliferation and activation of both naive and memory CD8+ T cells.6 Most recently, IL-21 has been demonstrated to exert a critical function in Th17 development.2,3,7 Interleukin-22,

this website a member of the IL-10 family, plays an important role in host defence, inflammation and tissue repair.8–10 It signals through a receptor complex, IL-22R1/IL-10R2.11 The IL-22R1 is expressed specifically on epithelial and some fibroblast cells in peripheral tissues such as gastrointestinal, respiratory system and skin but not on immune cells.12 Expression of IL-22 is augmented in many autoimmune diseases. The up-regulation of IL-22 is detected in Crohn’s disease, NVP-BEZ235 solubility dmso ulcerative colitis, psoriatic skin and preclinical mouse inflammatory bowel disease models. Studies in the mouse Klebsiella pneumonia infection model and mouse Citrobacter rodentium infection model support the essential role of IL-22 in mucosal immunity for the control of various infections.9,10 Our previous study and other reports demonstrate that IL-22 may play a role in the defence against fungal infections such as Candida

albicans.8,13 It may also play a role in tumour progression; it has been reported that IL-22 potentiated the expression of inducible nitric oxide synthase in human colon carcinoma cells.14 Our results showed that IL-21 induced

human naive CD8+ T cells to differentiate into Tc22 cells via phosphorylation of STAT1, STAT3 and STAT5. Moreover, IL-21 promoted the proliferation and IL-21R expression of activated naive CD8+ T cells, which suggests a positive feedback loop in the amplification of the IL-22+ CD8+ T cells. Umbilical cord blood was collected from healthy full-term newborn infants at the Secondary Affiliated Hospital of Sun Yat-sen University. Healthy volunteers between the ages of 20 and 26 years were recruited from Sun Yat-sen University. Adequate informed consent was obtained from all individuals involved in this study. The study was approved by the Medical School Review Board Ribose-5-phosphate isomerase at Sun Yat-sen University, China. The following antibodies were used for cell surface and intracellular stainings as well as for cell culture: CD8-allophycocyanin (APC), CD4-FITC, CD4-peridinin chlorophyll protein (PerCP), interferon-γ (IFN-γ) -APC, IFN-γ-FITC, GranzymB-FITC, phosphor-STAT1-phycoerythrin (PE), phosphor-STAT3-PE, phosphor-STAT4-FITC, phosphor-STAT5-FITC, phosphor-STAT6-APC, isotype-matched control antibodies, purified anti-CD3 and anti-CD28 monoclonal antibodies were purchased from BD Bioscience PharMingen (San Jose, CA). The IL-17-PE was purchased from eBioscience (Santiago, Chile) and IL-22-APC, IL-22-PE and IL-21R-PE were purchased from R & D Systems (Minneapolis, MN). We separated mononuclear cells from the cord blood of newborns as naive cells.