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Th1 Cytokines (th1 + cytokine)
Terms modified by Th1 Cytokines Selected AbstractsFunctional characterization of T cells differentiated in vitro from bone marrow-derived CD34+ cells of psoriatic patients with family historyEXPERIMENTAL DERMATOLOGY, Issue 8 2010Kaiming Zhang Please cite this paper as: Functional characterization of T cells differentiated in vitro from bone marrow-derived CD34+ cells of psoriatic patients with family history. Experimental Dermatology 2010; 19: e128,e135. Abstract Background:, The strong but complex genetic background suggests that inherent and intrinsic rather than exogenous factors have a key role in immunopathogenesis of psoriasis. It is reasonable to speculate that the dysfunctional activity of psoriatic T cells may partly originate from the abnormal haematopoietic cells. Objectives:, To test if T cells originated from haematopoietic progenitor cells in psoriasis patients display functional alternations similar to previously reported abnormalities of circulating T cells. Methods:, Bone marrow CD34+ haematopoietic cells were isolated from psoriatic patients with family history and healthy subjects, and differentiated into T cells in vitro in the thymic stromal co-culture system. These cells were further subjected to functional comparisons such as in vitro proliferation, secretion of cytokines such as IL-4, IL-8 and IFN,,, and inducing the production of C-myc, Bcl-xL, and Ki67 proteins in human keratinocytes. Results:, While bone marrow-derived CD34+ cells from both patients and healthy volunteers developed into mature T cells within weeks in the thymic environment in vitro, the differentiated T cells from psoriatic patients showed higher proliferation and stronger capacity to secret TH1 cytokines in response to streptococcal superantigen. The differentiated T cells from psoriatic patients, but not from normal controls, induced overexpression of C-myc and Ki67, but not Bcl-XL, in keratinocytes. Conclusions:, T cells differentiated from CD34+ cells of psoriatic patients, but not normal controls, are functionally similar to psoriatic circulating T cells, suggesting that the dysfunctional activity of T cells in psoriatic patients can be traced back to the early development of haematopoietic cells. [source] Th1 cytokine,induced downregulation of PPAR, in human biliary cells relates to cholangitis in primary biliary cirrhosis,HEPATOLOGY, Issue 6 2005Kenichi Harada Peroxisome proliferator-activated receptor-, (PPAR,) is known to inhibit the production of proinflammatory cytokines. In Th1-predominant diseases, PPAR, ligands can ameliorate clinical severity by downregulating the expression of proinflammatory cytokines. Primary biliary cirrhosis (PBC) is characterized by chronic destructive cholangitis with a Th1-predominant cytokine milieu. Unusual immune responses to infectious agents are suspected to underlie its etiopathogenesis. We examined the significance of PPAR, in biliary inflammation in connection to PBC. To this end, we performed immunohistochemistry, quantitative polymerase chain reaction, and nuclear factor-kappaB (NF-,B) DNA-binding assays to clarify the intrahepatic distribution of PPAR, and the regulation of PPAR, by inflammatory cytokines and PPAR, ligand in five cultured biliary cell lines including one derived from PBC liver. In liver specimens from patients with PBC, PPAR, protein was ubiquitously expressed in intrahepatic biliary epithelium, whereas the expression of PPAR, protein and mRNA was reduced in damaged bile ducts. PPAR, expression in cultured cells was upregulated by interleukin-4 (IL-4; Th2-type), but downregulated by IFN-, (Th1-type). PPAR, ligand negatively modulated lipopolysaccharide-induced NF-,B activation. Moreover, this inhibitory effect of PPAR, ligand was attenuated by pretreatment with IFN-,. In conclusion, PPAR, may be important to maintain homeostasis in the intrahepatic biliary epithelium, and its reduction in the bile ducts of PBC liver may be associated with the Th1-predominant milieu and with the development of chronic cholangitis in PBC. Immunosuppression using PPAR, ligands may be of therapeutic benefit to attenuate biliary inflammation in PBC. (HEPATOLOGY 2005;41.) [source] Influence of a cocoa-enriched diet on specific immune response in ovalbumin-sensitized ratsMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 3 2009Teresa Pérez-Berezo Abstract Previous studies in young rats have reported the impact of 3 weeks of high cocoa intake on healthy immune status. The present article describes the effects of a longer-term cocoa-enriched diet (9 weeks) on the specific immune response to ovalbumin (OVA) in adult Wistar rats. At 4 weeks after immunization, control rats produced anti-OVA antibodies, which, according their amount and isotype, were arranged as follows: IgG1 > IgG2a > IgM > IgG2b > IgG2c. Both cocoa diets studied (4% and 10%) down-modulated OVA-specific antibody levels of IgG1 (main subclass associated with the Th2 immune response in rats), IgG2a, IgG2c and IgM isotypes. Conversely, cocoa-fed rats presented equal or higher levels of anti-OVA IgG2b antibodies (subclass linked to the Th1 response). Spleen and lymph node cells from OVA-immunized control and cocoa-fed animals proliferated similarly under OVA stimulation. However, spleen cells from cocoa-fed animals showed decreased interleukin-4 secretion (main Th2 cytokine), and lymph node cells from the same rats displayed higher interferon-, secretion (main Th1 cytokine). These changes were accompanied by a reduction in the number of anti-OVA IgG-secreting cells in spleen. In conclusion, cocoa diets induced attenuation of antibody synthesis that may be attributable to specific down-regulation of the Th2 immune response. [source] Inflammatory cytokine gene expression in the urinary sediment of patients with lupus nephritisARTHRITIS & RHEUMATISM, Issue 5 2003Rebecca Wing-Yan Chan Objective Lupus nephritis is characterized by intrarenal inflammation and lymphocyte activation. In the present study, the expression of cytokine genes in the urinary sediment of patients with systemic lupus erythematosus (SLE) was examined. Methods We studied 3 SLE patient groups (25 with active lupus nephritis [active group], 25 with inactive SLE and previous renal involvement [remission group], 20 with inactive SLE and no history of renal involvement [nonrenal SLE group]) and 2 control groups (10 patients with noninflammatory renal diseases [non-SLE group] and 10 healthy volunteers [healthy group]). Cytokine gene expression in the urinary sediment was studied by real-time quantitative polymerase chain reaction. Results Expression of interferon-, (IFN,) in urinary sediment was significantly higher in the active group than in all other groups (P < 0.001 by Kruskal-Wallis test). Among the SLE patient groups, there was a close correlation between IFN, expression and the overall SLE Disease Activity Index (SLEDAI) score (Spearman's r = 0.590, P < 0.001) and the SLEDAI renal score (r = 0.642, P < 0.001). Urinary expression of interleukin-2 (IL-2) in the active group was significantly higher than that in the healthy group (P = 0.046) but not in the remission or nonrenal SLE groups. There was no difference in the levels of IL-4 expression among the SLE groups. Conclusion We found a predominance of Th1 cytokine in the urinary sediment of patients with active lupus nephritis. Measurement of cytokine gene expression in urinary sediment may be a useful noninvasive tool for assessing the severity of renal involvement in SLE. [source] Caspase-dependent and -independent apoptosis of mast cells induced by withdrawal of IL-3 is prevented by Toll-like receptor,4-mediated lipopolysaccharide stimulationEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 8 2003Hideshi Yoshikawa Abstract IL-3-dependent mucosal-like mast cells undergo apoptosis upon withdrawal of IL-3. Generally, the apoptosis is mediated by the activation of caspases and inhibited by addition of the pan-caspase inhibitors z-VAD-FMK or BOC-D-FMK. However, DNA fragmentation, a typical characteristic of apoptosis, is not inhibited by z-VAD-FMK or BOC-D-FMK in mast cell apoptosis. In this study, we demonstrate that the apoptosis of mast cells is mediated by both caspase-dependent and -independent mechanisms. The caspase-independent apoptosis is mediated by the translocation of endonuclease,G from mitochondria into nuclei. Withdrawal of IL-3 caused down-regulation of Bcl-xL, resulting in a drop in mitochondrial membrane transition potential followed by the release of cytochrome,c and endonuclease,G from mitochondria. However, stimulation of mast cells through Toll-like receptor,4 (TLR4) by lipopolysaccharide prevented mast cell apoptosis by inducing expression of Bcl-xL. Moreover, the activation of mast cells by LPS is enhanced in the presence of IFN-,, which up-regulates the expression of cell surface TLR4. Taken together, these observations provide evidence that mast cells play importantroles not only in allergic reactions but also in innate immunity recognizing enterobacteria through TLR4, and are regulated differently from allergic inflammation by Th1 cytokines. [source] Deficient translocation of c-Rel is associated with impaired Th1 cytokine production in T cells from atopic dermatitis patientsEXPERIMENTAL DERMATOLOGY, Issue 1 2005Karsten Dieckhoff Abstract:, Decreased production of T helper type 1 (Th1) cytokines, such as interferon-, (IFN-,) or interleukin-2 (IL-2), is a hallmark of atopic diseases. While accessory signals from antigen-presenting cells may be missing, T cells themselves may be suppressed in their ability to produce substantial amounts of Th1 cytokines. We show, in this study, that T cell receptor (TCR)-activated T cells from atopic dermatitis (AD) patients proliferate less than control T cells and produce lower amounts of IFN-, and IL-2, but comparable amounts of IL-4. Because mice lacking the nuclear factor kappa B (NF-,B) transcription factors , p65 or c-Rel , show reduced Th1, but undisturbed Th2 responses, we investigated the role of c-Rel and p65 for Th1 cytokine production in T cells from healthy and severe AD patients. TCR-activated primary T cells from healthy donors treated with c-Rel antisense oligonucleotides produced lower levels of IL-2 and IFN-, and proliferated less efficiently than the corresponding control T cells. Moreover, transfection of primary T cells with c-Rel or p65 enhanced proliferation and production of IL-2 and IFN-,. Nuclear extracts of activated primary T cells from AD donors bound weakly to NF-,B-specific oligonucleotides, compared to extracts from healthy control T cells. Western blotting studies revealed that nuclear, but not cytosolic, extracts from T cells of AD patients lacked significant amounts of c-Rel and p65. T cell clones derived from AD patients failed to sufficiently translocate c-Rel and p65 into the nucleus following activation. Thus, impaired nuclear translocation of c-Rel and p65 may determine an impaired Th1 cytokine response in AD. [source] Granulocyte colony-stimulating factor produces a decrease in IFN, and increase in IL-4 when administrated to healthy donorsJOURNAL OF CLINICAL APHERESIS, Issue 4 2010Octavio Rodríguez-Cortés Abstract Hematopoietic stem cells transplantation (HSCT) is the leading curative therapy for a variety of hematological and hereditary diseases; however, graft versus host disease (GVHD), an immunologic phenomenon that is favored by Th1 cytokines and cytotoxic cells from donors, is present frequently and is one of the most important causes of transplant related mortality. Peripheral blood HSCT is the preferred source of stem cells in almost 100% of the cases of autologous HSCT and in 70% of allogeneic transplants. The best mobilizing agent to get the stem cells out from the bone marrow is the Granulocyte-Colony Stimulating Factor (G-CSF). In this work, our main objective was to study a possible correlation between the graft cell dose and the patient's clinical outcome. We evaluated the immunologic changes produced by G-CSF in the lymphocyte and cytokine profiles in allogeneic HSC donors. HSC from twelve donors were mobilized with G-CSF at 16 ,g/kg/day, for 5 days. Basal Peripheral Blood (BPB), Mobilized Peripheral Blood (MPB), and aphaeresis mononuclear cells (G-MNC) samples were taken from all donors. Using flow cytometry, we quantified CD19+, CD3+, CD3+CD4+, CD3+CD8+, NK, NKT, DC1, and DC2 cells. Cytokines were determined by ELISA in culture supernatants. CD19+ (p = 0.001), DC1 (p < 0.002) and DC2 (p < 0.001) cells were increased in MPB with respect to BPB. An increase in Th2 cytokines such as (IL-4) and a decrease in Th1 cytokines (IFN,, IL-2) were also found in MPB samples. In conclusion, Th1 and Th2 cytokines are relevant in predicting the clinical outcome after allogeneic peripheral blood HSCT. J. Clin. Apheresis 25:181,187, 2010. © 2010 Wiley-Liss, Inc. [source] Th1 cytokines in oral lichen planusJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 2 2003Ambereen Khan Abstract Background:, Cell-mediated immune responses in oral lichen planus (OLP) may be regulated by cytokines and their receptors. Methods:,In situ cytokine expression and in vitro cytokine secretion in OLP were determined by immunohistochemistry and ELISA. Results:, The majority of subepithelial and intraepithelial mononuclear cells in OLP were CD8+. In some cases, intraepithelial CD8+ cells were adjacent to degenerating keratinocytes. CD4+ cells were observed mainly in the deep lamina propria with occasional CD4+ cells close to basal keratinocytes. Mononuclear cells expressed IFN-, in the superficial lamina propria and TNF-, adjacent to basal keratinocytes. Basal keratinocytes expressed TNF-, as a continuous band. TNF R1 was expressed by mononuclear cells and basal and suprabasal keratinocytes. There was variable expression of TGF-,1 in the subepithelial infiltrate while all intraepithelial mononuclear cells were TGF-,1,. Keratinocytes in OLP stained weakly for TGF-,1. Unstimulated OLP lesional T cells secreted IFN-,in vitro. TNF-, stimulation down-regulated IFN-, secretion and up-regulated TNF-, secretion. IL-4, IL-10 and TGF-,1 secretion were not detected. Conclusions:, These data suggest the development of a T helper 1 immune response that may promote CD8+ cytotoxic T-cell activity in OLP. [source] The immunological basis of psoriasisJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 2003C E M Griffiths ABSTRACT Evidence that psoriasis is an immune-mediated disorder comes from laboratory studies, clinical observation, and use of targeted therapies. Immunohistochemical studies have shown that the majority of T cells in psoriatic plaques are CD45RO+ memory-effector T cells that migrate into skin in recognition of an as yet undetermined antigen. There is also a predominance of Th1 cytokines, namely interferon gamma, in psoriatic plaques, in contrast to the predominance of Th2 cytokines found in atopic dermatitis. The efficacy of therapeutic agents that target T cells, such as anti-CD4+ monoclonal antibodies, cyclosporin, and interleukin-2 fusion toxin, has provided further substantial evidence that psoriasis is a T-cell-mediated disease. New T-cell targeted approaches and cytokine modulation are advancing basic science in providing an understanding of the evidence for the importance of the immune process in the biology of psoriasis. [source] IL-4,/, mice with lethal Mesocestoides corti infections , reduced Th2 cytokines and alternatively activated macrophagesPARASITE IMMUNOLOGY, Issue 12 2009A. E. O'CONNELL Summary Protection against Mesocestoides corti, a cestode that invades vital organs, is dependent on the production of IL-4, as IL-4,/, mice were found to have higher parasite burdens when compared with wild-type mice. The goal of this study was to investigate the role of IL-4 in immunity to M. corti, focusing on the immunological profile and on potential mediators of pathology. IL-4,/, mice infected with M. corti showed 100% mortality by 32 days, whereas wild-type mice survived for approximately 1 year. Parasite burdens were significantly increased in the liver, peritoneal, and thoracic cavities of IL-4,/, mice, associated with impaired recruitment of inflammatory cells and a reduction in monocytes and macrophages. IL-5 production by splenocytes and expression in liver tissue was decreased in infected IL-4,/, mice compared with wild-type mice. In contrast, IL-4,/, mice produced increased amounts of IFN, and TNF,. Alternatively activated macrophages were a major feature of liver granulomas in wild-type mice evidenced by Arginase I expression, while livers from infected IL-4,/, mice showed impaired alternative macrophage activation without increased classical macrophage activation. Thus, lethality during M. corti infection of IL-4,/, mice is associated with decreased Th2 cytokines, increased Th1 cytokines and impairment of alternatively activated macrophages. [source] Cytokine responses in immunized and non-immunized calves after Ostertagia ostertagi infectionPARASITE IMMUNOLOGY, Issue 9 2005E. CLAEREBOUT SUMMARY The objective of this study was to evaluate abomasal cytokine responses in helminth-naive calves and calves vaccinated with protective antigen fractions from Ostertagia ostertagi after an experimental challenge infection with infective third stage (L3) larvae. Abomasal lymph nodes and/or abomasal mucosa were collected and messenger RNA for the Th1 cytokines (IFN-,, IL-2, IL-12 p40 subunit), the Th2 cytokines (IL-4, IL-5, IL-6, IL-10, IL-13, IL-15) and the Th3/Tr cytokine TGF-, was quantified by real-time RT-PCR. Vaccination had no effect on cytokine profiles in either the abomasal lymph nodes or the abomasal mucosa. However, following infection all calves showed a significant decrease in the Th1 cytokines, IFN-, and IL-12 p40, and a significant increase in the Th2 cytokines, IL-4, IL-5, IL-10 and IL-13 in the lymph nodes, compared to non-infected calves. No correlation between the Th2 response and protection induced by vaccination could be demonstrated. In contrast, a Th2 pattern was not observed in the mucosa of the infected calves, which exhibited an increase in IFN-, as well as in the Th2 cytokines IL-4, IL-5 and IL-10 mRNA. No significant association was observed in the abomasal mucosa between any examined cytokine mRNA level and immune effector responses such as parasite-specific antibodies or the number of mucosal mast cells or eosinophils. [source] Altered cytokine profiles in patients with Chuvash polycythemia,AMERICAN JOURNAL OF HEMATOLOGY, Issue 2 2009Xiaomei Niu Chuvash polycythemia results from a homozygous 598C>T mutation in exon 3 of the von Hippel-Lindau (VHL) gene. This disrupts the normoxia pathway for degrading hypoxia inducible factor (HIF)-1, and HIF-2, causing altered expression of HIF-1 and HIF-2 inducible genes. As hypoxia induces expression of pro-inflammatory cytokines, we hypothesized that there might be an elevation of Th1 cytokines in the setting of Chuvash polycythemia. We analyzed plasma concentrations of Th1 (interleukins-2 and 12, interferon-,, granulocyte-monocyte colony-stimulating factor, tumor necrosis factor-,) and Th2 cytokines (interleukins-4, 5, 10, and 13) using the Bio-Plex multiplex suspension array system in 34 VHL598C>T homozygotes and 32 VHL wild-type participants from Chuvashia. Concentrations of all the Th1 and Th2 cytokines measured were elevated in the VHL598C>T homozygotes compared with the control wild-type participants, but the ratios of Th1 to Th2 cytokines did not differ by genotype. In parallel, peripheral blood concentrations of CD4 positive T-helper cells and CD4/CD8 ratio were lower in the VHL598C>T homozygotes. In conclusion, the up-regulated hypoxic response in Chuvash polycythemia is associated with increased plasma products of both the Th1 and Th2 pathways, but the balance between the two pathways seems to be preserved. Am. J. Hematol., 2009. © 2008 Wiley-Liss, Inc. [source] REVIEW ARTICLE: Effects of Early Conceptus Signals on Circulating Immune Cells: Lessons from Domestic RuminantsAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2010Troy L. Ott Citation Ott TL, Gifford CA. Effects of early conceptus signals on circulating immune cells: lessons from domestic ruminants. Am J Reprod Immunol 2010 While there are few similarities between mechanisms for extending corpus luteum (CL) function during early pregnancy in ruminants and primates, there is increasing evidence that conceptus-immune crosstalk in ruminants and primates affects the function of circulating immune cells at the very earliest stages of pregnancy. Most notable are changes in immune cell phenotypes with increased numbers of cells exhibiting the T regulatory phenotype and suppression of Th1 cytokines that promote tolerance to paternal alloantigens. Until recently, interferon , produced by the ruminant trophectoderm was thought to act exclusively on the uterine endometrium; however, it is now clear that this unique embryonic interferon escapes the uterus and alters gene expression in the CL and in peripheral blood leukocytes (PBL). In fact, a large number of interferon-stimulated genes are now known to be increased during early pregnancy in PBL. What is not known is how this conceptus-immune system cross-talk affects maternal immune status outside the reproductive tract. It is attractive to hypothesize that some of these effects are designed to counter-balance progesterone-induced immunosuppression so as not to place the dam at a greater risk of infection on top of the tremendous stresses already induced by pregnancy. Furthermore, recent evidence suggests that pregnancy induced changes in peripheral immune cells may aid in orchestrating establishment of pregnancy. Existing evidence points toward a greater convergence of systemic immune responses to early pregnancy signaling between ruminants and primates. [source] TH1/TH2,3 Imbalance due to Cytokine-Producing NK, ,, T and NK-,, T Cells in Murine Pregnancy Decidua in Success or Failure of PregnancyAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2001DAVID A. CLARK PROBLEM: Recurrent spontaneous abortion in DBA/2-mated CBA/J mice has been attributed to the production of Th1 cytokines (tumor necrosis factor [TNF]-, and interferon [IFN]-,) by asialoGM1+ natural killer (NK) cells and V,1.1,6.3+ T cells that infiltrate decidua by day 6.5, during the peri-implantation period. Abortions can be prevented by a second population of V,1.1,6.3 cells, which infiltrate on day 8.5 of gestation, and produce the Th2 cytokine interleukin (IL)-10 and Th3 cytokine transforming growth factor (TGF)-,2. In low abortion rate immunocompetent mice, most of the TGF-,2 is derived from ,, T cells. However, TGF-,2-producing cells are present in the decidua of pregnant severe combined immune deficient (SCID) mice, which lack ,, T cells. METHODS: The cells in day 13.5 decidua of CBA×DBA/2 matings and SCID×SCID matings were identified using flow cytometry and combined surface staining for ,, and/or asialoGM1, and intracellular cytokine staining for TNF-,, IFN-,, and TGF-,2,3. RESULTS: TGF-,2 and TNF-, were found in asialoGM1+ NK cells in SCID mouse decidua. In CBA×DBA/2 mated mice, two major and one minor subsets of cytokine-positive cells were identified: -,,-only T cells, double positive asialoGM1+,,+ (NK-,, T) cells, and a small number of asialoGM1+,,, NK-only cells. The NK-only and NK-,, T subsets showed a greater Th1/Th2,3 pattern of intracellular staining compared with the ,,-only subset. In the CBA×DBA/2 and SCID×SCID systems, Th1/Th2,3 ratios could not predict actual observed abortion rates but did correlate with susceptibility to abortions (if exposed to an additional stimulus such as stress). The known effect of in vivo administration of anti-asialoGM1 antibody on abortion rates within groups of mice exposed to such stresses could also be predicted. CONCLUSION: ,,+ cells in decidua (e.g. V,1+ cells which can recognize trophoblasts) differ based on the presence or absence of the NK marker-asialo-GM1. NK-,, T cells may be quite important in the Th1 response in early pregnancy that predisposes to abortions in CBA×DBA/2 matings, whereas ,, T-only cells appear to be protective. In pregnant SCID mice, the TNF-,+/TGF-,2+ NK population is greatly expanded. An activating stimulus (such as stress or endotoxin) appears to be as important in triggering abortions, as is the Th1/Th2,3 ratio at the feto,maternal interface. [source] Toll-like receptor ligands as adjuvants in allergen-specific immunotherapyCLINICAL & EXPERIMENTAL ALLERGY, Issue 12 2005P. Johansen Summary Background Allergen-specific immunotherapy (SIT) leads to long-term amelioration of T-helper type 2 (Th2)-mediated allergic symptoms and is therefore recommended as a first line therapy for allergies. The major disadvantage of SIT is its low efficiency, requiring treatment over years. Objective In this study, we evaluated the potential of Toll-like receptor (TLR) ligands to facilitate Th1-type immune responses. Methods The immunogenicity and therapeutic potential of the major bee venom allergen phospholipase A2 (PLA2) combined with various TLR ligands were tested in mice and compared with immune responses induced by conventional aluminium-based preparations. Results Regarding total IgG against PLA2, TLR2/4-binding lipopolysaccharide and TLR3-binding polyriboinosinic polyribocytidylic (PolyI:C) were the superior adjuvants for prophylactic vaccination. However, TLR9-binding phosphorothioate-modified cytosine,guanosine-rich oligonucleotide (CpG), TLR-3-binding PolyI:C, and TLR2/6-binding peptidoglycan skewed the immune responses more towards IgG2a isotype and Th1 cytokines. Furthermore, in a therapeutic approach, CpG, PolyI:C and TLR7/8-binding 3M003 had immune modulating properties as they suppressed established IgE titres. Conclusion The potential of TLR ligands to adjuvate the immunogenicity of bee venom PLA2 and to skew the Th1,Th2 balance proved very heterogeneous. With respect to SIT, CpG, PolyI:C, and 3M003 were very promising. Hence, TLR ligands should be considered as adjuvants or immune modulators in SIT in human as to improve its efficiency regarding the Th1,Th2 balance of the immune response with a likely effect on therapy duration. [source] Differential immunomodulatory properties of Bifidobacterium logum strains: relevance to probiotic selection and clinical applicationsCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2007M. Medina Summary Modulation of host immunity is one of the proposed benefits of the consumption of probiotics. Nonetheless, comparative studies on the immunological properties that support the selection of strains of the same species for specific health benefits are limited. In this study, the ability of different strains of Bifidobacterium longum to induce cytokine production by peripheral blood mononuclear cells (PBMCs) has been evaluated. Live cells of all B. longum strains greatly stimulated regulatory cytokine interleukin (IL)-10 and proinflammatory cytokine tumour necrosis factor (TNF)-, production. Strains of the same species also induced specific cytokine patterns, suggesting that they could drive immune responses in different directions. The probiotic strain B. longum W11 stimulated strongly the production of T helper 1 (Th1) cytokines while B. longum NCIMB 8809 and BIF53 induced low levels of Th1 cytokines and high levels of IL-10. The effects of cell-surface components obtained by sonication of B. longum strains overall confirm the effects detected by stimulation of PBMCs with live cells, indicating that these components are important determinants of the immunomodulatory activity of B. longum. Genomic DNA of some strains stimulated the production of the Th1 and pro-inflammatory cytokines, interferon (IFN)-, and TNF-,, but not that of IL-10. None of the cell-free culture supernatants of the studied strains was able to induce TNF-, production, suggesting that the proinflammatory component of these strains is associated mainly with structural cell molecules. The results suggest that despite sharing certain features, some strains can perform a better functional role than others and their careful selection for therapeutic use is desirable. [source] | ||||||||||||||||||||||